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Basic and Bedside

Electrocardiography
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Basic and Bedside

Electrocardiography

Romulo F. Baltazar, MD, FACC

Director, Noninvasive Cardiology
Sinai Hospital of Baltimore
Assistant Professor, Medicine
Johns Hopkins University
Baltimore, Maryland
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Acquisitions Editor: Frances Destefano

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Library of Congress Cataloging-in-Publication Data

Baltazar, Romulo F.
Basic and bedside electrocardiography / Romulo F. Baltazar.
p. ; cm.
Includes index.
ISBN-13: 978-0-7817-8804-5
ISBN-10: 0-7817-8804-8
1. Electrocardiography. I. Title.
[DNLM: 1. Electrocardiography. 2. Heart Diseasesdiagnosis. 3. Heart
Diseasestherapy. WG 140 B197b 2009]
RC683.5.E5B283 2009
616.1207547dc22
2008056135

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tents of the publication. Application of this information in a particular situation remains the profes-
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LWBK271-FM_i-x.qxd 1/29/09 1:58 PM Page v LWBK271-C01_01-08.qxd

This book is dedicated to my wife, Ophelia,

for her inspiration, support and encouragement in
the preparation of this book.
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M ore than 100 years since its introduction, electrocar-
diography continues to provide invaluable clinical
information. Even with the development of modern and
more expensive technologies, its significance has not de-
clined. To the contrary, its clinical application continues
to expand, and presently, it is the most utilized diagnostic
modality in the whole practice of medicine. In the hospi-
tal setting, it is routinely used to monitor both cardiac and
noncardiac patients, especially in acute care units and
during the performance of various cardiac and noncar-
diac procedures. Thus, the information provided by the
electrocardiogram should be standard knowledge for
every medical and paramedical professional who is in-
volved with patient care.
This book is purposely written in a format that will
assist the beginner, including medical students, nurses,
and paramedical professionals, in understanding basic
electrocardiography. It is also intended for interns, resi-
dents, physician assistants, fellows, anesthesiologists, and
clinical cardiologists by including standard of care treat-
ment of patients with electrocardiographic abnormalities
based on the most recent practice guidelines when guide-
lines are available. Thus, the book is a combination of
both basic and bedside electrocardiography.
The book integrates the comments and suggestions of
many interns, residents, and attending physicians to
whom I owe a great deal of gratitude. I would like to thank
Drs. Miruais Hamed, Paul Aoun, Eileen Zingman, Olga
Szalasny, Katja Vassiliades, Manish Arora, Onyi Onuoha,
Brandon Togioka, Darshana Purohit, Ranjani Ra-
manathan, Binu Matthew, Paolo Caimi, Mulugeta Fissha,
Hany Bashandy, Cindy Huang, Suzan Fattohy, Rachel
Preface
Hartman, Kevin Hayes, Khawaja Farook, Jason Javillo,
Jennifer Morales, Ubadullah Sharief, Ledys de Marsico,
Celian Valero, Samarina Ahmad, Kweku Hayford, Haritha
Pendli, Maya Morrison, and many others. I am also grate-
ful to Kittane Vishnupriya for his very helpful comments
and for the ECG that he painstakingly obtained to illus-
trate the significance of the posterior leads in the diagno-
sis of posterolateral myocardial infarction when he was a
coronary care resident. I am also grateful to Drs. Gabriela
Szabo, Ameena Etherington, and Soma Sengupta for re-
viewing chapters in the book, and Laura Baldwin, our su-
perb cardiology technician, who has taught me how to re-
trieve and record electrocardiograms from our archives.
I am also grateful to Dr. Morton Mower who has been
my mentor since I was a resident. His suggestions for im-
proving the book are greatly appreciated. I would also like
to express my deep appreciation to Dr. Steven Gambert,
Chief of the Department of Medicine, Johns Hopkins
University/Sinai Hospital Program in Internal Medicine,
for his support and encouragement and for his enthusi-
asm in having this book published.
Finally, I am grateful to my daughter, Cristina, who is
instrumental in teaching me how to use the computer in
the preparation of this book and my son Romulo, Jr who
decided on Radiology as his specialty, for his comments
and suggestions for simplifying some of the chapters,
especially those dealing with Basic Electrocardiography.
Romulo F. Baltazar, MD, FACC
Director, Noninvasive Cardiology, Department of Medicine
Johns Hopkins University/Sinai Hospital Program in
Internal Medicine
vii
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Contents

Preface vii

1 Basic Anatomy and Electrophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2 Basic Electrocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
3 The Lead System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
4 The Electrical Axis and Cardiac Rotation . . . . . . . . . . . . . . . . . . . . . . . . . 30
5 Heart Rate and Voltage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
6 Depolarization and Repolarization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
7 Chamber Enlargement and Hypertrophy . . . . . . . . . . . . . . . . . . . . . . . . . 62
8 Atrioventricular Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
9 Intraventricular Conduction Defect: Fascicular Block . . . . . . . . . . . . . . 112
10 Intraventricular Conduction Defect: Bundle Branch Block . . . . . . . . . . 120
11 Intraventricular Conduction Defect: Trifascicular Block . . . . . . . . . . . . 138
12 Sinus Node Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
13 Premature Supraventricular Complexes . . . . . . . . . . . . . . . . . . . . . . . . . 167
14 Sinus Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180
15 Supraventricular Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
16 Supraventricular Tachycardia due to Reentry . . . . . . . . . . . . . . . . . . . . . 187
17 Supraventricular Tachycardia due to Altered Automaticity . . . . . . . . . . 211
18 Atrial Flutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
19 Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246
20 Wolff-Parkinson-White Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262
21 Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287
22 Wide Complex Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310
23 Acute Coronary Syndrome: ST Elevation Myocardial Infarction . . . . . . 331
24 Acute Coronary Syndrome: Non-ST Elevation Myocardial
Infarction and Unstable Angina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379
25 Electrolyte Abnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 396
26 The ECG of Cardiac Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 414

Appendix: Commonly Used Injectable Pharmacologic Agents . . . . . . . . . . . . . 435

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 449
ix
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1
Basic Anatomy and
Electrophysiology

Basic Anatomy of the Heart The Sinus Node and Intraventricular

Conduction System
The cardiac chambers: The heart is the center of the
circulatory system and is the organ that pumps blood The sinus node and conduction system: The heart
to the different parts of the body. It consists of two up- has a generator that gives rise to an electrical impulse
per receiving chambersthe right atrium and left and an electrical circuit; this allows the cardiac impulse
atriumand two lower pumping muscular cham- to propagate from atria to ventricles in an orderly se-
bersthe right ventricle and left ventricle (Fig. 1.1). quence. The generator of the heart is the sinus node
Right atrium: The right atrium receives venous and the electrical circuit is the intraventricular conduc-
blood from the different parts of the body through tion system (Fig. 1.2A, B).
the superior and inferior vena cavae and directs the Intraventricular conduction system: The bundle of
blood to the right ventricle. His, right and left bundle branches, the fascicular
Right ventricle: The right ventricle pumps blood branches of the left bundle branch, and Purkinje fibers
to the pulmonary artery for delivery to the lungs. constitute the intraventricular conduction system.
Left atrium: The left atrium receives oxygenated Their cells are specialized for rapid and orderly con-
blood from the lungs through four separate pul- duction of the electrical impulse and may be regarded
monary veins and delivers blood to the left ventricle. as the electrical circuit of the heart.
Left ventricle: The left ventricle pumps oxygenated
blood to the aorta for delivery to the different parts
of the body.
Basic Anatomy of the Heart
Superior
vena cava From Lungs
Sinus node: The sinus node is the origin of the cardiac
Pulmonary
vein
impulse and is the pacemaker of the heart. It is located
Right Left high within the right atrium near the entrance of the
atrium atrium superior vena cava.
Atria: The atria consist of a thin layer of muscle cells
Inferior
that conduct the sinus impulse directly to the atrioven-
Right Left
vena cava Ventricle ventricle tricular (AV) node. The atria also contracts upon ar-
rival of the impulse from the sinus node. With contrac-
tion of the atria, additional blood is pumped to the
Pulmonary Aorta ventricles.
artery AV node: The AV node is the only pathway through
To Systemic
To Lungs Circulation which the sinus impulse can reach the ventricles. It is
located at the floor of the right atrium, adjacent to
Figure 1.1: Anatomy of the Heart. Diagrammatic the ventricular septum. The AV node slows down the
representation of the heart showing two upper receiving conduction of the sinus impulse to the ventricles so
chambersthe right and left atriaand two lower muscular that contraction of the atria and ventricles does not
pumping chambersthe right and left ventricles. Arrows point occur simultaneously. This results in a better cardiac
to the direction of blood flow. output.
1
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2 Chapter 1

Figure 1.2: The Sinus Node and the Sinus Node

Intraventricular Conduction System
of the Heart. (A) Diagrammatic repre- Atria
sentation of the sinus node, atria, AV node, Sinus
and the intraventricular conduction sys- Node
Left bundle AV Node
tem of the heart. (B) Diagram showing AV RA LA
branch
the sequence of conduction of the cardiac Node
impulse from sinus node to the ventricles. Bundle of His
His Left
AV, atrioventricular; BB, bundle branch; bundle posterior
LA, left atrium; LV, left ventricle; RA, right fascicle Right BB Left BB
atrium; RV, right ventricle. Right RV LV
bundle
Left
branch Left Left
anterior
fascicle anterior posterior
fascicle fascicle
Purkinje
fibers
Purkinje
A fibers Purkinje fibers

Right Left
Ventricle Ventricle
B

Bundle of His: The AV node continues into the bundle
of His, a short structure that immediately divides into
two main branches: the left and right bundle branches.
Right bundle branch: The right bundle branch is a
long and thin branch of the His bundle that courses to
the right side of the ventricular septum. It terminates
into a network of Purkinje fibers in the endocardium of
the right ventricle.
Left bundle branch: The left bundle branch is a short
branch of the His bundle that spreads to the left side of
the ventricular septum in a fanlike fashion forming
three distinct fascicles.
Left anterior fascicle: This fascicle courses to the
anterior and superior walls of the left ventricle.
Midseptal fascicle: This fascicle branches to the
ventricular septum and is intricately connected with
the anterior and posterior fascicles.
Left posterior fascicle: This fascicle courses to the
posterior and inferior walls before terminating in a
network of Purkinje fibers.
Purkinje system: The Purkinje system is the terminal
portion of the conduction system consisting of a net-
work of fibers within the endocardium of both ventri-
cles. It spreads the impulse directly to the my-
ocardium, causing both ventricles to contract in
synchrony.
Ventricles: The ventricles are the main pumping cham-
bers of the heart. Because the muscles of the ventricles
are the thickest structure in the heart, they generate the
largest deflection in the electrocardiogram (ECG).
Basic Electrophysiology
Basic electrophysiology: The heart consists of three
special types of cells with different electrophysiologic
properties (Fig. 1.3). These cells include:
Muscle cells: Muscle cells are specialized for con-
traction and are present in the atria and ventricles.

Figure 1.3: Action Potential of a 1

1 1
Muscle Cell, Conducting Cell and 2 2 2
0 0 0
Pacemaking Cell. The action potential
of a ventricular muscle cell specialized for 3 3 3
0 0 0
contraction (A), His-Purkinje cell special- 4
ized for impulse conduction (B), and 4
4 4 4 4
sinus node cell with special properties of - 90 mv - 60 mv
automaticity (C). - 95 mv
A: Muscle Cell B: Conducting Cell C: Pacemaking Cell
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+20 mV
1 2
0 mV
Depolarization
0
Repolarization
3
0 Rest
4 4
- 90 mv
Figure 1.4: Action Potential of a Ventricular Muscle
Cell. The action potential of a ventricular muscle cell is shown.
Phase 4 corresponds to the resting potential, which is approxi-
mately 90 mV. When the cell is depolarized, the potential
abruptly changes from 90 mV to 20 mV and is represented
by a rapid upstroke or phase 0. Phase 1 returns the overshoot to
neutral. Phase 2 corresponds to the plateau phase in which the
potential is maintained at 0 mV for a constant duration. Phase
3 returns the potential rapidly to resting baseline of 90 mV.
Conducting cells: Conducting cells are specialized
for rapid conduction of the electrical impulse and
are present within the entire His-Purkinje system.
Pacemaking cells: Pacemaking cells have proper-
ties of automaticity and are capable of generating
electrical impulses. These cells are present in the si-
nus node and throughout the His-Purkinje system.
All myocardial cells are electrically polarized with
the inside of the cell more electrically negative than
the outside. This negative potential is due to the dif-
ference in concentration of electrolytes inside the
cell compared with outside. Because the cells are po-
larized, they are capable of being discharged. When
the cells are discharged, an action potential is gener-
ated. Recordings of action potentials of a ventricular
muscle cell, conducting cell from the His-Purkinje
system and a pacemaking cell from the sinus node
are shown in Figure 1.3.
Action potential of a ventricular muscle cell: When
a ventricular muscle cell discharges, an action potential
is generated. A recorded action potential is shown in
Figure 1.4. The action potential can be divided into five
separate phases: 0, 1, 2, 3, and 4. Taken together, the five
phases of the action potential represent a complete
electrical cycle with phase 0 representing depolariza-
tion, phases 1 to 3 representing repolarization, and
phase 4 representing rest or quiescence.
Phase 4: A ventricular muscle cell has a resting po-
tential of approximately 90 mV, meaning the cell is
more negative inside than outside by about 90 mV.
This is primarily because of the higher concentra-
tion of potassium inside the cell than outside. This
resting state corresponds to phase 4 of the action
potential.
Phase 0: Depolarization of the cell corresponds to
phase 0 of the action potential. During phase 0, the
Basic Anatomy and Electrophysiology 3
polarity of the cell changes rapidly from 90 mV to
0 mV, transiently overshooting the point of equilib-
rium by 20 mV. This rapid depolarization is due to
the transit of positively charged sodium from out-
side the cell to inside and is represented by the rapid
upstroke of the action potential.
Phase 1: This corresponds to the return of the over-
shoot to 0 mV.
Phase 2: This corresponds to the plateau phase of
the action potential, which is maintained at approx-
imately 0 mV.
Phase 3: This is due to rapid repolarization return-
ing the polarity of the cell immediately to its resting
potential of 90 mV.
Action potential of sinus node cell: The action po-
tential of a sinus node cell, which is a pacemaker cell, is
different from a muscle cell. The features of a pace-
maker cell that make it different from a nonpacemak-
ing cell are summarized in the diagram (Fig. 1.5).
Spontaneous depolarization: The most important
difference between a pacemaker and a non-pace-
maker cell is that during phase 4, cells with pacemak-
ing properties exhibit slow spontaneous diastolic de-
polarization, which is characterized by a slowly rising
upward slope of the resting potential. This is due to
slowly decreasing negativity of the cell caused by the
slow entry of sodium ions into the cell. Because
sodium carries positive charges, the cell becomes less
and less negative until it reaches a certain threshold
(threshold potential), above which the cell automati-
cally discharges. This property is not present in non-
pacemaking cells because non-pacemaking cells have
flat or very slow rising diastolic slopes during phase 4,
which never reach threshold potential.
Resting potential: The resting potential of a sinus
node cell is approximately 60 mV and therefore is
less negative than the resting potential of a ventric-
ular muscle cell, which is approximately 90 mV.
This causes phase 0 to rise slowly resulting only in
a small overshoot of 0 to 10 mV (see Fig. 1.5) as
compared with that seen in the non-pacemaker
cell.
Repolarization: After the cells are depolarized, they
have to recover before the arrival of the next impulse.
This process of recovery is called repolarization. Re-
polarization is a longer process than depolarization
and includes phases 1, 2, and 3 of the action poten-
tial. During repolarization, the cell may not be able to
respond to another stimulus. The likelihood of re-
sponse depends on the electrical status of the cell
(Fig. 1.6).
Absolute refractory period: The cell is unable to
respond to any kind of stimulus during this period.
It includes phases 1 and 2.
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4 Chapter 1

Small and blunted

0 mv overshoot of 0-10 mV

Phase 0 is
Phase 4: Slow slow rising
spontaneous
0
depolarization
Threshold 3
Potential

- 40 mv
4 4 4
- 60 mv
Resting potential is -60 mV

Figure 1.5: Action Potential of a Sinus Node Cell. The action potential of a sinus
node cell is shown. The resting potential is approximately 60 mV and is less negative than
the resting potential of a ventricular muscle cell, which is approximately 90 mV. Slow spon-
taneous depolarization is present during phase 4. Phase 0 is slow rising with only a small
overshoot. These features differentiate a pacemaking cell from a non-pacemaking cell and
are highlighted.

Effective refractory period: The cell is able to gen-
erate a potential; however, it is too weak to be propa-
gated. This includes a small portion of phase 3.
Relative refractory period: The cell is partially re-
polarized and may be able to respond to a stimulus
if the stimulus is stronger than usual. This period in-
cludes a portion of phase 3 extending to threshold
potential, which is about 70 mV.
Basic Anatomy
Supernormal phase: The cell may respond to a
less than normal stimulus. This period includes the
end of phase 3 when repolarization is almost com-
1
2 These cells have properties of automaticity and are capable of
0
Absolute RP
3 neously, the cells in the sinus node have the fastest rate of dis-
Effective
Threshold 0 RP Relative RP
potential
4 Supernormal Period
- 90 mv
Repolarization (Phases 1-3)
Figure 1.6: Repolarization and Refractory Periods. Re-
polarization includes phases 1 to 3 of the action potential. The
absolute refractory period includes phases 1 and 2 in which the
cell cannot be stimulated by any impulse. The effective
refractory period includes a small portion of phase 3 in which a
stimulus can elicit a local response but not strong enough to be
propagated. Relative refractory period is that portion of phase 3
that extends to threshold potential. The cell will respond to a
stimulus that is stronger than normal. The supernormal phase
starts just below threshold potential where the cell can respond
to a stimulus that is less than normal. RP, refractory period.
plete and has reached a potential that is more nega-
tive than the threshold potential of 70 mV.
Basic Anatomy and
Electrophysiology
The sinus node: The sinus node is located in the superior
and lateral border of the right atrium. The most cranial por-
tion starts from the epicardium at the junction of the supe-
rior vena cava and right atrium. Its most caudal portion is lo-
cated subendocardially. The sinus node contains pacemaker
cells that are widely distributed throughout its entire length.
discharging spontaneously. Although there are other cells
in the heart that are also capable of discharging sponta-
charge. The sinus node therefore is the pacemaker of the
heart. The sinus node is supplied by the sinus node artery
that originates from the right coronary artery 60% to 65% of
the time. The rest of the vascular supply originates from the
left circumflex coronary artery.
Internodal tracts: There are three internodal tracts con-
necting the sinus node to the AV node namely the anterior,
posterior, and middle internodal tracts. The significance of
these internodal tracts is uncertain because the sinus impulse
is conducted to the AV node through the atria.
The AV node: The AV node is smaller than the sinus node
and is located in the lower right atrium just above the inser-
tion of the septal leaflet of the tricuspid valve and anterior to
the entrance of the coronary sinus to the lower right atrium.
The AV node consists of three areas with distinct properties:
the upper, middle, and lower portions. The upper portion
also called AN (atrionodal) region connects the atria to the
LWBK271-C01_01-08.qxd 1/29/09 11:25 AM Page 5 LWBK271-C01_01-08.qxd
middle portion, which is called N (nodal) region. The lower
portion, also called NH (nodo-His) region, connects with
the bundle of His. The middle region is primarily responsible
for delaying AV conduction. It is also where acetylcholine is
released. It has no automatic properties in contrast to the up-
per and lower regions, which contain cells with properties of
automaticity. In 90% of patients, the AV node is supplied by
the AV nodal artery, which is a branch of the right coronary
artery. In the remaining 10%, the AV node artery comes from
the left circumflex coronary artery.
The His-Purkinje system: The AV node continues as the
His bundle, which immediately divides into the right and the
left bundle branches. The right bundle branch is a direct con-
tinuation of the bundle of His and continues down the right
side of the interventricular septum toward the right ventric-
ular apex and base of the anterior papillary muscle. The left
bundle branch fans into several branches. These branches
can be grouped into three main subdivisions or fascicles: the
anterior, midseptal, and posterior fascicles. These fascicles
are interconnected with each other. The significance of the
midseptal fascicle is uncertain, although it is probably re-
sponsible for the initial depolarization of the ventricular sep-
tum. The right bundle branch and the fascicles end into a
network of Purkinje fibers over the endocardial surface of
both ventricles. Conduction across the His-Purkinje system
is not significantly affected by sympathetic and parasympa-
thetic influences. The blood supply of the His bundle comes
from both anterior and posterior descending coronary arter-
ies through their septal branches.
Basic Electrophysiology
There are three special types of cells in the heart, each with its
own distinctive electrophysiologic property. They include
muscle cells such as those of the atria and ventricles, con-
ducting cells such as those of the His-Purkinje system, and
pacemaking cells such as those of the sinus node.
All cells are polarized with the inside of the cell more nega-
tive than the outside. This difference in the electrical charge
is due to the different concentration of electrolytes inside the
cell compared with outside. The major electrolytes that de-
termine the difference in gradient between the inside and
outside the cell are:
Potassiumthe concentration of K is 30 to 50 times
higher inside than outside the cell.
Sodiumthe concentration of Na is reversed from that
of potassium and is almost 10 times higher outside than
inside the cell.
Calciumthe concentration of Ca2 is higher outside
than inside the cell.
The cell membrane is relatively impermeable to electrolytes.
The movement of ions into and out of the cell membrane is
controlled by channels that are specific to certain ions. Na
channels are present that are specific only for sodium ions.
K and Ca2 channels are also present that are specific only
Basic Anatomy and Electrophysiology 5
for potassium and calcium ions, respectively. These ions,
however, cannot enter into and out of the cell any time. The
channels open and close only at given moment. In other
words, they are gated. The voltage of the cell membrane con-
trols the gates; thus, opening and closing of these channels
are voltage sensitive. Channels that are specific only for
sodium ions, called fast sodium channels, are closed when
the potential or voltage of the cell is 90 mV (resting poten-
tial). The fast sodium channels will open only when the cell is
depolarized, resulting in rapid entry of sodium ions into the
cell. This corresponds to the rapid upstroke (phase 0) of the
action potential.
The Action Potential of Muscle Cells in the
Atria and Ventricles
The sodium pump: The resting potential of muscle cells in
the ventricles is approximately 90 mV. It is slightly less in
the atria. During the resting state, the cell membrane is im-
permeable to sodium. A higher concentration of sodium is
maintained outside the cell compared with inside the cell,
because of the presence of a Na/K pump located in the cell
membrane. The Na/K pump exchanges three Na ions
from inside the cell for two K ions outside the cell. This ex-
change process requires energy, which is derived from the hy-
drolysis of adenosine triphosphate by the enzyme sodium-
potassium adenosine triphosphatase (ATPase). Because there
are three ions of Na exchanged for two ions of K, a positive
ion is lost during the exchange making the inside of the cell
more negative.
The increasing negativity of the cell when Na is ex-
changed for K is due to the presence of large negatively
charged proteins inside the cell. These large proteins are
unable to diffuse out of the cell because of their size.
Thus, when three ions of Na exit the cell in exchange for
two ions of K entering the cell, the large proteins will
have one negative charge that is not neutralized, making
the inside of the cell more negative until a potential of 90
mV is reached.
Mechanism of action of digitalis: If the Na/K AT-
Pase pump is inhibited, sodium is removed through the
Na/Ca2 exchange mechanism. Sodium inside the cell is
exchanged for calcium, which causes calcium to accumu-
late within the cell. This increase in intracellular calcium
through inhibition of the Na/K ATPase pump is the
mechanism by which digitalis exerts its inotropic effect.
In the presence of digitalis toxicity, this exchange can con-
tinue even after the cell has completed its repolarization
(beyond phase 3). This may cause the potential of the cell
to become transiently less negative, resulting in delayed
afterdepolarization. Such afterdepolarizations do not al-
ways reach threshold potential. In the case when thresh-
old potential is reached, it may result in repeated oscilla-
tions of the cell membrane and can cause tachycardia due
to triggered activity.
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6 Chapter 1
An action potential has five phasesphases 0, 1, 2, 3, and 4.
A complete electrical cardiac cycle includes depolarization
(which corresponds to phase 0), repolarization (phases 1, 2,
and 3), and a period of rest or quiescence (corresponding to
phase 4 of the action potential).
Phase 0: Phase 0 corresponds to the very rapid upstroke
of the action potential.
n Phase 0 starts when the muscle cell is depolarized by
the sinus impulse, which is propagated from one cell to
the next adjacent cell. When the cell is depolarized, the
fast Na channels in the cell membrane are activated,
allowing sodium ions to enter the cell. Because sodium
ions are positively charged, they neutralize the negative
ions making the potential inside the cell less negative.
After the threshold potential of approximately 70 mV
is reached, all fast sodium channels open, allowing
sodium, which is approximately 10 to 15 times higher
outside than inside the cell, to enter rapidly. The explo-
sive entry of Na into the cell is the cause of the rapid
upstroke of the action potential where the polarity of
the cell not only becomes neutral (0 mV) but will re-
sult in an overshoot of approximately 20 to 30 mV.
n The entry of Na into the cell occurs only over a frac-
tion of a second, because the fast sodium channel
closes immediately when the membrane potential be-
comes neutral. After the fast sodium channel closes, it
cannot be reactivated again and will not reopen until
the potential of the cell is restored to its original rest-
ing potential of 90 mV.
n Depolarization or phase 0 of the action potential is
equivalent to the R wave (or QRS complex) of a single
myocardial cell. Because there are millions of myocar-
dial cells within the ventricles that are simultaneously
depolarizing, it will take approximately 0.06 to 0.10
seconds to depolarize all the myocardial cells in both
ventricles. This period corresponds to the total dura-
tion of the QRS complex in the surface ECG. Thus,
when there is left ventricular hypertrophy or when
there is bundle branch block, the duration of the QRS
complex becomes wider because it will take longer to
activate the entire ventricle.
n After depolarization, the cell has to repolarize so that
it can prepare itself for the next wave of excitation.
Repolarization includes phases 1 to 3 of the action po-
tential.
Phase 1: Early rapid repolarization starts immediately af-
ter phase 0, with the return of the polarity of the cell from
approximately 20 to 30 mV to almost neutral (0 mV).
n The decrease in potential from 20 to 30 mV to 0
mV is due to the abrupt closure of fast sodium chan-
nels and transient activation of the potassium chan-
nels causing outward movement of K. This transient
outward movement of potassium is more prominent
in the epicardium compared with endocardium,
which may explain the shorter action potential dura-
tion of epicardial cells compared with endocardial
cells. This difference in action potential duration is
clinically important because this can favor reentry
(see Brugada syndrome, Chapter 23, Acute Coronary
SyndromeST Elevation Myocardial Infarction).
n In the surface ECG, phase 1 and early phase 2 coin-
cides with the J point, which marks the end of the
QRS complex and beginning of the ST segment.
Phase 2: Phase 2 represents the plateau phase in which
the potential of the cell remains unchanged at approxi-
mately 0 mV for a sustained duration.
n The opening of the fast sodium channels during phase
0 of the action potential is also accompanied by the
opening of the calcium channels when the voltage of
the cell has reached approximately 40 mV. Unlike the
fast sodium channel that opens and closes transiently,
the flow of calcium into the cell is slower but is more
sustained. Because the cell membrane is much more
permeable to potassium ions than to other ions and
because there is a much higher concentration of
potassium inside than outside the cell, potassium
leaks out of the cell (loss of positive ions), counterbal-
ancing the entry of calcium into the cell (gain of pos-
itive ions). These two opposing forces maintain the
polarity of the cell in equilibrium at approximately 0
mV for a sustained duration that corresponds to the
plateau of the action potential.
n The entry of calcium into the cell also triggers the re-
lease of more calcium from storage sites in the sar-
coplasmic reticulum. This calcium-triggered calcium
release mechanism is responsible for initiating con-
traction of the muscle cell. Throughout the duration
of phase 2, the cells in the ventricles remain in a sus-
tained state of contraction. During this period, the
cells remain absolutely refractory and cannot be depo-
larized by an external stimulus.
n Phase 2 corresponds to the ST segment in the ECG,
which normally remains isoelectric throughout its du-
ration.
Phase 3: Phase 3 represents rapid ventricular repolariza-
tion. During phase 3, the polarity of the cell becomes
more negative until it reaches its original resting potential
of 90 mV.
n The increasing negativity of the cell during phase 3 is
due to inactivation of the calcium channels with de-
creased entry of calcium into the cell. However, the ef-
flux of potassium out of the cell continues, making the
potential of the cell more negative until it reaches 90
mV. After the resting potential of 90 mV is reached,
repolarization of the cell is complete, and the cell is
again ready to be depolarized.
n Phase 3, or rapid ventricular repolarization, corre-
sponds to the T wave in the ECG. The end of the re-
polarization period corresponds to the end of the T
wave and marks the beginning of phase 4.
LWBK271-C01_01-08.qxd 1/29/09 11:25 AM Page 7 LWBK271-C01_01-08.qxd
Phase 4: Phase 4 represents the resting or quiescent state
of the myocardial cell. The polarity of the cell when repo-
larization is completed is approximately 90 mV.
n During the resting state, the K channels in the cell
membrane are open while the channels of other ions
remain closed. Because of the much higher concentra-
tion of K inside than outside the cell, outward flow of
K continues. The loss of K ions increases the nega-
tivity inside the cell. As the potential of the cell be-
comes more negative, an electrical force is created that
attracts the positively charged potassium ions back
into the cell against its concentration gradient. Thus,
during phase 4, two forces acting in opposite directions
cause the K ions either to migrate in (because of elec-
trical force) or migrate out (because of difference in
K concentration across the cell membrane) until a
steady state is reached where migration of the K into
and out of the cell reaches an equilibrium. This corre-
sponds to the final resting potential of a ventricular
muscle cell, which is approximately 90 mV. This rest-
ing electrical potential can be predicted for potassium
using the Nernst equation, where the resting potential
of the cell is influenced by the difference in concentra-
tion of K across the cell membrane and by the electri-
cal forces attracting K back into the cell.
n In ventricular muscle cells, phase 4 is maintained con-
stantly at approximately 90 mV, making the slope
relatively flat. The muscle cell can be discharged only
by an outside stimulus, which is the arrival of the
propagated sinus impulse.
n Phase 4 corresponds to the T-Q interval in the ECG.
This interval is isoelectric until it is interrupted by the
next wave of depolarization.
Conducting Cells of the His-Purkinje System
The His-Purkinje system is specialized for rapid conduction.
The action potential of the His-Purkinje cells is very similar to
that of atrial and ventricular muscle cells except that the rest-
ing potential is less negative at approximately 95 mV. The
more negative the action potential, the faster is the rate of rise
of phase 0 of the action potential. This results in a more rapid
(steeper) slope of phase 0, a higher overshoot and a more pro-
longed duration of the action potential. This explains why
conduction of impulses across the His-Purkinje fibers is ap-
proximately five times faster than ordinary muscle cells.
Pacemaker Cells in the Sinus Node
Pacemaker cells in the sinus node and AV junction have
properties of automaticity. These cells can discharge sponta-
neously independent of an outside stimulus. Muscle cells in
the atria and ventricles, in contrast, do not possess the prop-
erty of automaticity. However, they may develop this prop-
erty if they are injured or become ischemic.
Basic Anatomy and Electrophysiology 7
The action potentials of automatic cells of the sinus node
and AV node differ from those of non-pacemaker cells. Most
importantly, they demonstrate a slow spontaneous diastolic
depolarization during phase 4 of the action potential. These
differences are discussed next.
Phase 4:
n During phase 4, the resting potential of the automatic
cells exhibit spontaneous depolarization. The poten-
tial of the pacemaker cell becomes less and less nega-
tive until it reaches threshold potential. This decreas-
ing negativity of the resting potential is called slow
spontaneous diastolic depolarization. This is the most
important property that differentiates a pacemaking
cell from a non-pacemaking cell. The non-pacemak-
ing cell has a flat diastolic slope during phase 4 and
does not exhibit slow spontaneous depolarization.
Thus, the potential of the non-pacemaking cell never
reaches threshold.
n The presence of spontaneous diastolic depolarization
is due to the presence of sodium channels that are
open during diastole. These sodium channels are not
the same as the fast sodium channels that are respon-
sible for phase 0 of the action potential. They are acti-
vated immediately after the cell reaches its most nega-
tive potential, causing sodium ions to enter the cell
slowly. This slow entry of sodium into the cell is called
pacemaker or funny current. This renders the polarity
of the cell during phase 4 less and less negative until
the threshold potential is reached.
n Also during phase 4, the resting potential of pacemak-
ing cells of the sinus node measures approximately
50 to 60 mV and is therefore less negative than the
resting potential of atrial and ventricular muscle cells,
which measures approximately 90 mV. This less neg-
ative potential of no more than 50 to 60 mV causes
the fast sodium channel to be inactivated perma-
nently. The resting potential of the cell has to be re-
stored to 90 mV before the fast sodium channels can
be activated. Thus, phase 0 of the action potential of
the sinus node and pacemaking cells of the AV junc-
tion is not due to the entry of sodium through fast
sodium channels, but is mediated by the entry of cal-
cium into the cell. After phase 4 reaches threshold po-
tential, which is approximately 40 mV, the calcium
channels open, resulting in the entry of calcium into
the cell, which causes phase 0 of the action potential.
n Among all cells of the heart with pacemaking proper-
ties, the cells in the sinus node have the fastest rate of
rise during phase 4 of the action potential. This ac-
counts for why the sinus node has the fastest cyclical
rate per minute and is the pacemaker of the heart.
Other cells with automatic properties can be found in
parts of the atria, AV junction, His-Purkinje system,
and muscle cells of the mitral and tricuspid valves.
Although these cells also exhibit slow diastolic depo-
LWBK271-C01_01-08.qxd 1/29/09 11:25 AM Page 8 LWBK271-C01_01-08.qxd
8 Chapter 1
larization, the rate of rise of the diastolic slope of
phase 4 of these cells is much slower. Thus, these cells
will be discharged by the propagated sinus impulse
before their potential can reach threshold potential.
n There is an hierarchical order in the AV conduction
system in which cells that are closest to the AV node
have the fastest rate of rise during phase 4 of the ac-
tion potential compared with cells that are located
more distally. Thus, when the sinus node fails as the
pacemaker of the heart, cells in the AV node at its
junction with the bundle of His usually come to the
rescue because these automatic cells have the fastest
rate compared with other potential pacemakers of the
heart.
Phase 0:
n As previously mentioned, the fast sodium channels do
not play any role in triggering phase 0 of the action
potential in the pacemaker cells of the sinus node and
AV junction since the resting potential of these cells
are not capable of reaching 90 mV. Thus, the fast
sodium channels remain closed and do not contribute
to phase 0 of the action potential.
n Depolarization of the cell occurs through calcium
channels that open when the resting potential of the
cell spontaneously reaches 40 mV.
n Because the resting potential is less negative at 60
mV and phase 0 is mediated by calcium ions, the rate
of rise of phase 0 is slower. This results in a slope that
is less steep with a lower overshoot than that of mus-
cle cells of the atria and ventricles.
Refractory Periods
The myocardial cell needs to repolarize before the arrival of
the next impulse. If complete repolarization has not been
achieved, the cell may or may not respond to a stimulus, de-
pending on the intensity of the stimulus and the extent to
which the cell has recovered at the time the stimulus is deliv-
ered. Not surprisingly, refractory periods are defined accord-
ing to the phase of the action potential at which the impulse
arrives.
Absolute refractory period: The absolute refractory
period is the period in the action potential during which
the cell cannot respond to any stimulus. This period in-
cludes phase 1 and phase 2 of the action potential.
Effective refractory period: The effective refractory pe-
riod is the period during which the cell can be stimulated;
however, the action potential that is generated is not
strong enough to propagate to other cells. This period in-
cludes a short interval of phase 3 (approximately 25 mV).
Relative refractory period: The relative refractory pe-
riod starts from the end of the effective refractory period
and extends to a potential slightly less negative than 70
mV, which is the threshold potential. Not all of the fast
sodium channels are fully recovered at this time. Thus, the
potential generated has a lower amplitude and a slower
rate of rise of phase 0 of the action potential. The impulse
will still be propagated but conduction velocity is slower.
Supernormal period: The cell may respond to less than
ordinary stimuli if the cell is stimulated at a potential that
is slightly below (more negative than) its threshold poten-
tial of 70 mV. The potential of the cell would therefore
be only a few millivolts from becoming threshold poten-
tial. Thus, a smaller than normal stimulus is sufficient to
excite the cell. This short interval corresponds to the su-
pernormal period of repolarization.
Suggested Readings
Conover MB. Normal electrical activation of the heart. In: Un-
derstanding Electrocardiography. 8th ed. St. Louis: Mosby;
2003:822.
Dunn MI, Lipman BS. Basic physiologic principles. In: Lipman-
Massie Clinical Electrocardiography. 8th ed. Chicago: Year-
book Medical Publishers Inc; 1989:2450.
Greineder K, Strichartz GR, Lilly LS. Basic cardiac structure and
function. In: Lilly LS, ed. Pathophysiology of Heart Disease.
2nd ed. Baltimore: Lippincott Williams & Wilkins; 1993:
1 23.
Shih H-T. Anatomy of the action potential in the heart. Texas
Heart J. 1994;21:3041.
LWBK271-C02_09-22.qxd 1/29/09 1:51 PM Page 9 LWBK271-C01_01-08.qxd
Basic Electrocardiography
The Normal Sinus Impulse
The sinus node is the origin of the normal electrical
impulse. Although there are other cells in the heart that
can also discharge spontaneously, the sinus node has
the fastest rate of discharge and is the pacemaker of the
heart.
Normal Sinus Rhythm: Any impulse originating from
the sinus node is called normal sinus rhythm. The sinus
node discharges at a rate of 60 to 100 beats per minute
(bpm), although the rate could vary depending on the
metabolic needs of the body.
Sinus bradycardia: When the rate of the sinus
node is 60 bpm, the rhythm is called sinus brady-
cardia.
Sinus tachycardia: When the rate is 100 bpm,
the rhythm is called sinus tachycardia.
Sinus arrhythmia: When the sinus impulse is ir-
regular, the rhythm is called sinus arrhythmia.
The electrical impulse that is generated from the sinus
node spreads from the atria to the ventricles in an or-
derly sequence. In this manner, contraction of the atria
and ventricles is closely synchronized to maximize the
efficiency of the heart as a pump (Fig. 2.1).
Sinus
Node
Left
Right
Atrium Atrium
AV Node
Bundle of His
Right
Left Bundle
Bundle
Ventricles
2
Activation of the AtriaThe P Wave
The Sinus Impulse: When the sinus node discharges,
no deflection is recorded because the impulse from the
sinus node is not strong enough to generate an electri-
cal signal. The first deflection that is recorded after the
sinus node discharges is the P wave.
P Wave: The P wave is the first deflection in the electro-
cardiogram (ECG) and is due to activation of the atria.
Configuration: The configuration of the normal si-
nus P wave is smooth and well rounded. Because the
sinus node is located at the upper border of the right
atrium, the sinus impulse has to travel from the right
atrium to the left atrium on its way to the ventricles.
The first half of the P wave therefore is due to activa-
tion of the right atrium (Fig. 2.2A). The second half
is due to activation of the left atrium (Fig. 2.2B).
Duration: The width or duration of the normal
sinus P wave measures 2.5 small blocks (0.10
seconds). This is the length of time it takes to acti-
vate both atria.
Amplitude: The height or amplitude of the normal
sinus P wave also measures 2.5 small blocks
(0.25 mV).
Figure 2.1: Diagrammatic Representa-
tion of the Sinus Node and Conduction
System. The sinus node is the origin of
the normal electrical impulse and is the pace-
maker of the heart. The sinus impulse spreads
to the atria before it is propagated to the
Intraventricular ventricles through the atrioventricular node
Conduction
and special conduction system.
System
9
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10 Chapter 2

Figure 2.2: Atrial Activation The initial half of The terminal half
the P Wave. When the sinus node the P wave is due of the P wave is
discharges, no electrical activity is to activation of due to activation
recorded in the electrocardiogram. the right atrium of the left atrium
The first deflection is the P wave,
which represents activation of the
atria. The initial half of the P wave Left Right
Right Left
represents activation of the right atrium atrium atrium
atrium
atrium and the terminal half repre-
sents activation of the left atrium.

Ventricles Ventricles

A B

and fascicles, which constitute the intraventricular con-

Activation of the Atrioventricular Node
After depolarization of the atria, the only pathway by
which the sinus impulse can reach the ventricles is
through the atrioventricular (AV) node and intraven-
tricular conduction system.
The AV node: The AV node consists of a network of
special cells that normally delay conduction of the
atrial impulse to the ventricles. As the impulse traverses
the AV node on its way to the ventricles, it does not
generate any electrical activity in the ECG. Therefore,
an isoelectric or flat line is recorded immediately after
the P wave (Fig. 2.3).
Intraventricular Conduction System
After the impulse emerges from the AV node, it is con-
ducted rapidly through the His bundle, bundle branches,
duction system, before terminating in a branching net-
work of Purkinje fibers. The spread of the electrical im-
pulse in the His-Purkinje system also does not cause any
deflection in the ECG, similar to that of the AV node. This
is represented as a continuation of the isoelectric or flat
line after the P wave.
Activation of the Ventricles
The QRS Complex
QRS Complex: The QRS complex represents activa-
tion of the ventricles. The QRS complex generates
the largest deflection in the ECG because the ventri-
cles contain the largest mass of muscle cells in the
heart, collectively referred to as the myocardium
(Fig. 2.4).

AV node His-Purkinje system

Figure 2.3: Activation of the
Atrioventricular Node and His-
Purkinje System. Propagation of the No electrical activity is recorded in the ECG as
the impulse traverses the AV node, His bundle,
impulse at the atrioventricular node bundle branches, fascicles and Purkinje fibers
and His-Purkinje system will not cause
any deflection in the electrocardiogram
and is represented as an isoelectric or
flat line after the P wave. AV Node

Left bundle branch

His bundle
Left posterior fascicle
Right bundle Left anterior fascicle
branch

Purkinje fibers
LWBK271-C02_09-22.qxd 1/29/09 1:51 PM Page 11 LWBK271-C01_01-08.qxd
The QRS complex represents
simultaneous activation of both
ventricles
Figure 2.4: Activation of the Ventriclesthe QRS
Complex. Activation of the ventricles is represented as a QRS
complex in the electrocardiogram. Because the Purkinje fibers
are located in the endocardium, the endocardium is the first to
be activated. The impulse spreads from endocardium to
epicardium in an outward direction. Arrows point to the direc-
tion of activation.
The spread of the sinus impulse through the His-
Purkinje system is very rapid and efficient, but is
electrically silent with no impulse recorded in the
ECG. The QRS complex is recorded only when
the impulse has spread from the Purkinje fibers to
the myocardium.
The myocardium can be arbitrarily divided into
three layers: the endocardium, which is the inner
layer, the mid-myocardium, and the epicardium,
which is the outer layer of the myocardium.
The Purkinje fibers are located in the endocardium
of both ventricles. Because the electrical impulse
arrives first at the Purkinje fibers, the ventricles are
activated from endocardium to epicardium in an
outward direction.
The QRS complex corresponds to phase 0 of the ac-
tion potential of all individual myocardial cells of
both ventricles. Because the ventricles consist of a
thick layer of myocardial cells, not all cells are depo-
larized at the same time. Depolarization of the
whole myocardium can vary from 0.06 to 0.10
seconds or longer. This duration corresponds to the
width of the QRS complex in the ECG.
R R R R
r gram shows how the waves are identified
QS
q q
S
QS R qR RS rR
Basic Electrocardiography 11
The QRS Complex
QRS Complex: The QRS complex has various waves
that go up and down from baseline. These waves are
identified as follows: Q, R, S, R, and S. If additional
waves are present, R or S designations may be
added. Regardless of the size of the deflections, cap-
ital and small letters are used empirically mainly for
convenience, although, generally, capital letters des-
ignate large waves and small letters, small waves
(Fig. 2.5).
Q wave: The Q wave is defined as the first wave of
the QRS complex below the baseline. If only a deep
Q wave is present (no R wave), the QRS complex is
described as a QS complex.
R wave: The R wave is defined as the first positive
(upward) deflection of the QRS complex. If only an
R wave is present (no Q wave or S wave), the QRS
complex is described as an R wave.
S wave: The S wave is the negative deflection after
the R wave.
R: The R (R prime) is the next positive wave after
the S wave.
S: The S (S prime) is the next negative deflection
after the R.
R or S: These waves are rarely used, however if ad-
ditional waves are needed to describe the QRS com-
plex, the letter R (R double prime) is used for the
next positive wave and S (S double prime) for the
next negative wave.
QRS complex: The QRS complex is identified as a
QRS complex regardless of the number of waves
present. Thus, a tall R wave without a Q wave or S
wave is still identified as a QRS complex.
The J Point, ST Segment, and T Wave
The QRS complex is followed by a flat line called the ST
segment. The end of the QRS complex and beginning
of the ST segment is called the J point. The flat ST
segment is followed immediately by another positive
deflection called the T wave.
Figure 2.5: QRS Nomenclature. Dia-
r r r
in the QRS complex.
q
S S
qrS qrSr
LWBK271-C02_09-22.qxd 1/29/09 1:51 PM Page 12 LWBK271-C01_01-08.qxd
12 Chapter 2
J Point
T Wave
ST Segment
Figure 2.6: Repolarization of the Ventricles. Ventricular
repolarization begins immediately after depolarization and
starts at the J point, which marks the end of the QRS complex,
and extends to the end of the T wave. This corresponds to
phases 1, 2, and 3 of the action potential. Ventricular repolariza-
tion allows the ventricles to recover completely and prepares
the myocardial cells for the next wave of depolarization.
J point: The J point, also called the J junction,
marks the end of the QRS complex and beginning of
the ST segment (Fig. 2.6).
ST segment: The ST segment starts from the J
point to the beginning of the T wave. The ST seg-
ment is flat or isoelectric and corresponds to phase 2
(plateau phase) of the action potential of the ven-
tricular myocardial cells. It represents the time when
all cells have just been depolarized and the muscle
cells are in a state of sustained contraction. The ven-
tricular muscle cells are completely refractory dur-
ing this period and cannot be excited by an outside
stimulus.
T wave: The T wave represents rapid ventricular re-
polarization. This segment of ventricular repolar-
ization corresponds to phase 3 of the transmem-
brane action potential. During phase 3, the action
potential abruptly returns to its resting potential of
90 mV.
The J point, ST segment, and T wave represent the
whole process of ventricular repolarization correspon-
ding to phases 1, 2, and 3 of the transmembrane action
potential. Repolarization returns the polarity of the
myocardial cells to resting potential and prepares the
ventricles for the next wave of depolarization.
The PR Interval, QRS Complex,
and QT Interval
The duration of the PR interval, QRS complex, and QT
interval are routinely measured in the standard 12-lead
ECG. These intervals are shown in Figure 2.7.
PR interval: The PR interval is measured from the
beginning of the P wave to the beginning of the QRS
PR Interval QT Interval
P T
QRS Complex
Figure 2.7: The PR Interval, QRS Complex, and QT
Interval. The PR interval is measured from the beginning of
the P wave to the beginning of the QRS complex. The QRS com-
plex is measured from the beginning of the first deflection to the
end of the last deflection and the QT interval is measured from
the beginning of the QRS complex to the end of the T wave.
complex. If the QRS complex starts with a Q wave,
the PR interval is measured from the beginning of
the P wave to the beginning of the Q wave (P-Q in-
terval), but is nevertheless called PR interval. The
normal PR interval measures 0.12 to 0.20 seconds in
the adult. It includes the time it takes for the sinus
impulse to travel from atria to ventricles. The PR in-
terval is prolonged when there is delay in conduc-
tion of the sinus impulse to the ventricles and is
shortened when there is an extra pathway connect-
ing the atrium directly to the ventricle.
QRS complex: The QRS complex is measured from
the beginning of the first deflection, whether it starts
with a Q wave or an R wave, and extends to the end
of the last deflection. The normal QRS duration
varies from 0.06 to 0.10 seconds. The QRS duration
is increased when there is ventricular hypertrophy,
bundle branch block, or when there is premature
excitation of the ventricles because of the presence
of an accessory pathway.
The QT Interval
QT Interval: The QT interval includes the QRS com-
plex, ST segment, and T wave corresponding to phases
0 to 3 of the action potential. It is measured from the
beginning of the QRS complex to the end of the T
wave. Note that the presence of a U wave is not in-
cluded in the measurement. In assessing the duration
of the QT interval, multiple leads should be selected
and the QT interval is the longest QT that can be meas-
ured in the whole 12-lead ECG recording.
QTc: The QT interval is affected by heart rate. It be-
comes longer when the heart rate is slower and shorter
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QT interval (in seconds)
QTc =
R-R interval (in seconds)
R-R Interval
QT Interval
Figure 2.8: The QT Interval. The QT interval is measured
from the beginning of the QRS complex to the end of the T wave.
When the heart rate is 70 bpm, one can eyeball that the QTc is
normal if the QT interval is equal to or less than half the R-R inter-
val. When this occurs, no calculation is necessary. If the QT inter-
val is more than half the R-R interval, the QTc may not be normal
and should be calculated (see example in Fig. 2.9).
when the heart rate is faster. The QT interval therefore
should always be corrected for heart rate. The corrected
QT interval is the QTc.
The simplest and most commonly used formula for
correcting the QT interval for heart rate is the Bazett
formula shown here.
The normal QTc should not exceed 0.42 seconds in
men and 0.44 seconds in women. The QTc is pro-
longed when it measures 0.44 seconds in men and
0.46 seconds in women and children.
An easy rule to remember in calculating the QTc
when the heart rate is 70 bpm is that the QTc is
normal (0.46 seconds) if the QT interval is equal
to or less than half the R-R interval (Fig. 2.8).
QT interval (in seconds) 0.40
QTc = = =
R-R interval (in seconds) 0.75
R-R Interval = 14 Small Blocks
ECG
Action
Potential
QT Interval = 10 Small Blocks
Basic Electrocardiography 13
Calculating the QTc: Table 2.1 is useful in calculating
the QTc when a calculator is not available. In the example
in Figure 2.9, the short technique of visually inspecting
the QT interval can be used because the heart rate is 70
bpm. The QT interval (10 small blocks) is more than half
the preceding R-R interval (14 small blocks). Thus, the
QTc may not be normal and needs to be calculated.
First: Measure the QT interval: The QT interval
measures 10 small blocks. This is equivalent to 0.40
seconds (Table 2.1, column 1, QT interval in small
block).
Second: Measure the R-R interval: The R-R inter-
val measures 14 small blocks, which is equivalent to
0.56 seconds. The square root of 0.56 seconds is 0.75
seconds (see Table 2.1).
Finally: Calculate the QTc: Using the Bazett for-
mula as shown below: QTc  0.40  0.75  0.53
seconds. The QTc is prolonged.
Rapid calculation of the QTc using the Bazett formula
is shown below.
The Normal U Wave: The end of the T wave completes
the normal cardiac cycle, which includes the P wave,
the QRS complex, and the T wave. The T wave, how-
ever, may often be followed by a small positive deflec-
tion called the U wave. The U wave is not always pres-
ent, but it may be the last complex in the ECG to be
recorded (Fig. 2.10).
The size of the normal U wave is small, measuring
approximately one-tenth of the size of the T wave.
U waves are best recorded in the anterior precordial
leads V2 and V3 because these chest leads are closest
to the ventricular myocardium.
U waves are usually visible when the heart rate is
slow (65 bpm) and rarely visible with faster heart
rates (95 bpm).
Figure 2.9: Calculating the QTc. If a
0.53 sec calculator is not available, the QTc can be
calculated by using Table 2.1. The preced-
ing R-R interval is measured because the
QT interval is dependent on the previous
QT Interval
R-R interval. In this figure, the QT interval
(10 small blocks) is more than half the pre-
ceding R-R interval (14 small blocks), thus
the QTc may not be normal and should be
calculated as shown in the text. The right
1 2 panel is a reminder that the QT interval is
equivalent to the total duration of the
0 3
4 action potential (phases 0 to 3).
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14 Chapter 2

TABLE 2.1

Calculating the QTc QT interval 1sec 2

QTc 1sec 2 
2RR interval 1sec 2
QT Interval
R-R Interval Heart Rate R-R Interval Square Root of
QT (Small Blocks) QT (sec) (Small Blocks) (Beats per Minute) (sec) R-R Interval (sec)
45 1.80 45 33 1.80 1.34
44 1.76 44 34 1.76 1.33
43 1.72 43 35 1.72 1.31
42 1.68 42 36 1.68 1.30
41 1.64 41 37 1.64 1.28
40 1.60 40 38 1.60 1.26
39 1.56 39 39 1.56 1.25
38 1.52 38 39 1.52 1.23
37 1.48 37 41 1.48 1.22
36 1.44 36 42 1.44 1.20
35 1.40 35 43 1.40 1.18
34 1.36 34 44 1.36 1.17
33 1.32 33 45 1.32 1.15
32 1.28 32 47 1.28 1.13
31 1.24 31 48 1.24 1.11
30 1.20 30 50 1.20 1.10
29 1.16 29 52 1.16 1.08
28 1.12 28 54 1.12 1.06
27 1.08 27 56 1.08 1.04
26 1.04 26 58 1.04 1.02
25 1.00 25 60 1.00 1.00
24 0.96 24 63 0.96 0.98
23 0.92 23 65 0.92 0.96
22 0.88 22 68 0.88 0.94
21 0.84 21 71 0.84 0.92
20 0.80 20 75 0.80 0.89
19 0.76 19 79 0.76 0.87
18 0.75 18 83 0.75 0.87
17 0.68 17 88 0.68 0.82
16 0.64 16 94 0.64 0.80
15 0.60 15 100 0.60 0.77
14 0.56 14 107 0.56 0.75
13 0.52 13 115 0.52 0.72
12 0.48 12 125 0.48 0.69
11 0.44 11 136 0.44 0.66
10 0.40 10 150 0.40 0.63
9 0.36 9 167 0.36 0.60
8 0.32 8 188 0.32 0.57
7 0.28 7 214 0.28 0.53
Column 2 converts the measured QT interval to seconds; the last column converts the measured R-R interval to its square root.

A normal U wave is upright in all leads except aVR be-
cause the axis of the U wave follows that of the T wave.
The origin of the normal U wave is uncertain, al-
though it is believed to be due to repolarization of
the His-Purkinje system.
Abnormal U Wave: U waves are often seen in normal
individuals, but can be abnormal when they are
inverted or when they equal or exceed the size of the T
wave. This occurs in the setting of hypokalemia.
T-Q Segment: The T-Q segment is measured from
the end of the T wave of the previous complex to the
Q wave of the next QRS complex. It represents electri-
cal diastole corresponding to phase 4 of the action
potential.
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T-Q Segment
U
Figure 2.10: The U Wave and T-Q Segment. The U wave
is the last deflection in the electrocardiogram and is best
recorded in leads V2 and V3 because of the close proximity of
these leads to the ventricular myocardium. The cause of the
U wave is most likely the repolarization of the His-Purkinje
system. U waves are abnormal when they are inverted or become
unduly prominent, as may be seen in the setting of hypokalemia.
The T-Q segment corresponds to phase 4 of the action potential.
It marks the end of the previous action potential and the begin-
ning of the next potential.
Summary of ECG Deflections
See Figure 2.11.
P wave: The P wave represents activation of the atria.
PR interval: The PR interval starts from the beginning
of the P wave to the beginning of the QRS complex and
represents the time required for the sinus impulse to
travel from the atria to the ventricles.
PR segment: The PR segment starts at the end of the P
wave to the beginning of the QRS complex and corre-
sponds to the time it takes for the impulse to travel
from AV node to ventricles.
QRS complex: This represents activation of all the
muscle cells in the ventricles and corresponds to phase
0 of the action potential.
J point: The J point marks the end of the QRS complex
and beginning of the ST segment. It corresponds to
phase 1 of the action potential.
TQ Segment
QRS
P J Point
PR
Segment T U
PR Interval ST Segment
Basic Electrocardiography 15
ST segment: The ST segment is the isoelectric portion
between the J point and the beginning of the T wave. It
corresponds to phase 2 (plateau) of the action poten-
tial.
T wave: The T wave represents rapid repolarization of
the ventricles and corresponds to phase 3 of the action
potential.
QT: The QT interval is measured from the beginning of
the QRS complex to the end of the T wave and corre-
sponds to electrical systole.
TQ: The TQ segment starts from the end of the T wave
to the beginning of the next QRS complex. This repre-
sents phase 4 of the action potential and corresponds
to electrical diastole.
U wave: The U wave, if present, is the last positive de-
flection in the ECG. It is likely due to repolarization of
the His-Purkinje system.
Abnormal Waves in the ECG
There are other waves in the ECG that have been de-
scribed. These waves are not normally present but
should be recognized because they are pathologic and
diagnostic of a clinical entity when present.
Delta wave: The delta wave is a slow and slurred
upstroke of the initial portion of the QRS complex
and is usually seen in conjunction with a short PR
interval (Fig. 2.12A). Its presence is diagnostic of the
Wolff-Parkinson-White syndrome. Delta waves are
caused by an accessory pathway that connects the
atrium directly to the ventricles across the atrioven-
tricular groove resulting in pre-excitation of the
ventricles (see Chapter 20, Wolff-Parkinson-White
Syndrome).
Osborn wave: The Osborn wave, also called a J
wave, is a markedly exaggerated elevation of the J
point that results in an H shape configuration of
QT Interval Figure 2.11: Summary of the
Electrocardiogram Waves, Inter-
vals, and Segments.
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16 Chapter 2

Delta wave Epsilon wave

Osborn wave

A B C

Figure 2.12: Abnormal Waves in the electrocardiogram. (A) Delta waves char-
acterized by slowly rising upstroke of the QRS complex from preexcitation (Wolff-Parkinson-
White syndrome). (B) Osborn waves, which resemble an h because of hypothermia
and hypercalcemia. (C) Epsilon waves seen as extra notch after the QRS in V1, V2, or V3
diagnostic of arrhythmogenic right ventricular dysplasia.

the QRS complex. The presence of the Osborn wave

is associated with hypothermia or hypercalcemia
(Fig. 2.12B).
Epsilon wave: The epsilon wave is an extra notch
at the end of the QRS or early portion of the ST seg-
ment most commonly seen in V1 to V3. This extra
notch represents delayed activation of the outflow
tract of the right ventricle and is diagnostic of
arrhythmogenic right ventricular dysplasia, also
called arrhythmogenic right ventricular cardiomy-
opathy (Fig. 2.12C). Arrhythmogenic right ventric-
ular dysplasia is an inherited form of cardiomyopa-
thy characterized by the presence of fibro-fatty
infiltrates within the myocardium of the right ven-
tricle that can result in ventricular arrhythmias. It is
a common cause of sudden cardiac death in young
individuals.
Transmembrane Action Potential and
the Surface ECG
The diagram (Fig. 2.13) shows the relationship between
the action potential of a single ventricular myocardial
cell and the surface ECG. A complete cardiac cycle can
be divided into two phases: systole and diastole.
Systole: Systole corresponds to the QT interval and
includes:
n Depolarization: Depolarization is phase 0 of the
action potential. This is equivalent to the QRS
complex in the ECG.
n Repolarization: Repolarization includes phases
1, 2, and 3, which correspond to the J point, ST
segment, and T wave in the ECG.

Figure 2.13:The Transmembrane Action 1 1

Potential and the Surface Electro- 2
0
cardiogram. Transmembrane action potential
of a ventricular myocardial cell (A) and the corre-
sponding surface electrocardiogram (B). Phase 0 3
of the action potential is equivalent to the QRS 0 0
complex, phase 1 the J point, phase 2 the ST seg-
ment, phase 3 the T wave, and phase 4 the TQ seg- A
ment. Note that repolarization and depolarization 4 4
- 90 mv
of the myocardium occur during systole, which
corresponds to the QT interval. Diastole, which is QT Interval TQ Segment
phase 4, the rest period, corresponds to the TQ Phase 0-3 Phase 4
interval. Electrical Systole Electrical Diastole

J Point
(Phase 1)

P
B

ST Segment T Wave QRS

(Phase 2) (phase 3) (Phase 0)
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Basic Electrocardiography 17

Figure 2.14:Electrical and Mechanical

Aortic Aortic Valve
Valve Systole and Diastole. The electrocardio-
Closes (A2)
Opens gram (ECG), left ventricular, left atrial, and aor-
tic root pressure tracings are shown. Electri-
Aortic cal systole corresponds to the QT interval in
Pressure
the ECG. Mechanical systole starts from S1
Mitral Valve Mitral Valve
Closes (M1) Opens (first heart sound) because of closure of the
mitral (M1) and tricuspid (T1) valves, and ex-
Left Atrial Pressure
tends to S2 (second heart sound) because of
closure of the aortic (A2) and pulmonic (P2)
Left Ventricular
valves. There is a slight electromechanical de-
Pressure
lay from the onset of the QRS complex to the
Mechanical Systole
onset of S1. Electrical diastole is equivalent to
S1S2 Interval the TQ segment in the ECG. This is equivalent
to mechanical diastole, which starts from S2
and extends to S1.

ECG
Electrical Systole Electrical Diastole
QT Interval TQ Segment
Phonocardiogram
T AP
M1 1 2
2
M1T1
S1 S2 S1
Mechanical Systole Diastole

Diastole: Diastole occurs during phase 4, or the
resting period of the cell. This corresponds to the
TQ segment in the ECG.
Timing of Systole and Diastole
The 12-Lead ECG
It is important to recognize that the ECG represents
electrical events and that a time lag occurs before me-
chanical contraction and relaxation.
Systole: In the ECG, electrical systole starts with the
QRS complex and ends with the T wave correspon-
ding to the QT interval. At bedside, mechanical sys-
tole begins with the first heart sound or S1 and ends
with the second sound or S2 (Fig. 2.14).
Diastole: In the ECG, diastole starts at the end of
the T wave to the next Q wave (TQ). At bedside, di-
astole extends from S2 to S1.
Shown here are examples of complete 12-lead ECGs. A con-
tinuous lead II rhythm strip is recorded at the bottom of each
tracing. The first ECG (Fig. 2.15) is a normal ECG. The sec-
ond ECG (Fig. 2.16) shows prominent U waves in an other-
wise normal ECG.

Figure 2.15: Normal Electrocar-

diogram. The rhythm is normal
QRS sinus with a rate of 62 beats per
P T minute.
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18 Chapter 2
Figure 2.16: Prominent U
Waves. Twelve-lead electrocardio-
gram showing U waves in almost all
leads. U waves are usually seen when
the heart rate is slow and are most
prominent in the anterior precordial
leads because these leads are closest
to the ventricles. The U waves are
marked by the arrows.
The Normal Electrocardiogram
The ECG Deflections
1. The P wave represents activation of the atria.
2. The QRS complex represents activation of the ventricles.
3. The T wave represents rapid repolarization of the ventricles.
4. U wave represents repolarization of the His-Purkinje
system.
Segments and Intervals
1. PR interval represents the time it takes for the sinus impulse
to travel from the atria to the ventricles.
2. QT interval represents electrical systole and extends from the
onset of the QRS complex to end of the T wave.
3. The J point marks the end of the QRS complex and begin-
ning of the ST segment.
4. JT interval is the QT interval without the QRS complex.
5. The ST segment begins immediately after the QRS complex
and extends to the onset of the T wave.
6. TQ interval represents electrical diastole and extends from
the end of the T wave to the beginning of the next QRS
complex.
The ECG Deflections, Segments, and Intervals
and their Clinical Implications
The P wave: The sinus node does not leave any imprint
when it discharges. The P wave is the first deflection in the
ECG and indicates that the sinus impulse has spread to the
atria. The P wave therefore represents activation of the atria
and is the only ECG evidence that the sinus node has dis-
charged.
The sinus P wave
Because the sinus impulse is not represented in the ECG
when the sinus node discharges, the configuration of the
U wave
P wave is the main criterion in identifying that the im-
pulse is sinus or non-sinus in origin. The sinus node is lo-
cated at the right upper border of the right atrium close to
the entrance of the superior vena cava. Because of its
anatomic location, the sinus impulse has to travel from
right atrium to left atrium in a leftward and downward
(inferior) direction. This is represented in the ECG as an
upright P wave in leads I, II, and aVF, as well as in V3 to V6.
Lead II usually records the most upright P wave deflection
and is the most important lead in recognizing that the
rhythm is normal sinus. If the P wave is inverted in lead II,
the impulse is unlikely to be of sinus node origin.
The sinus impulse follows the same pathway every time it
activates the atria; thus, every sinus impulse has the same
P wave configuration.
The P wave duration should not exceed 2.5 small blocks
(0.10 seconds or 100 milliseconds). The height of the P
wave also should not exceed 2.5 small blocks (2.5 mm)
and is measured vertically from the top of the baseline to
the top of the P wave. The duration of the P wave represents
activation of the left and right atria. According to the Amer-
ican College of Cardiology/American Heart Association/
Heart Rhythm Society, the P wave duration should
be measured in at least three leads that are recorded
simultaneouslypreferably leads I, II, and V1from the
beginning of the P wave to the end of the P wave. The P
wave is abnormal when there is increased amplitude or
duration, when the shape of the wave is peaked, notched,
or bifid, or when it is inverted or absent in lead II.
n Increased duration of the P wave: A prolonged P
wave suggests enlargement of the left atrium or intra-
atrial block.
n Increased amplitude of the P wave: Increased P
wave amplitude suggests enlargement of the right
atrium.
Activation of the atria is immediately followed by atrial con-
traction. The mechanical contraction of the atria is not audi-
ble. However, when the ventricles are stiff or noncompliant,
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as occurs when there is left ventricular hypertrophy, a
fourth heart sound (S4) may be audible because of vibra-
tions caused by blood hitting the ventricular walls during
atrial contraction. A fourth heart sound may not be pres-
ent when there are no P waves; for instance, when the
rhythm is junctional or when there is atrial fibrillation.
Ta wave: The P wave may be followed by a repolarization
wave called the Ta wave. The Ta wave is the T wave of the
P wave. The Ta wave is small and is usually not visible be-
cause it becomes obscured by the coinciding QRS com-
plex. The direction of the Ta wave in the ECG is opposite
that of the P wave. Thus, when the P wave is upright, the
Ta wave is inverted.
The PR interval: The PR interval represents the time re-
quired for the sinus impulse to reach the ventricles. It in-
cludes the time it takes for the sinus impulse to travel
through the atria, AV node, bundle of His, bundle branches,
fascicles of the left bundle branch, and the Purkinje network
of fibers until the ventricles are activated.
The normal PR interval measures 0.12 to 0.20 seconds in
the adult. The PR interval is measured from the beginning
of the P wave to the beginning of the QRS complex. The
longest as well as the shortest PR interval in the 12-lead
ECG tracing should be measured so that delay in the con-
duction of the sinus impulse to the ventricles and prema-
ture excitation of the ventricles are not overlooked.
n Prolonged PR interval: The PR interval is prolonged
when it measures 0.20 seconds (200 milliseconds).
This delay in the conduction of the sinus impulse
from atria to ventricles is usually at the level of the AV
node. The whole 12-lead ECG is measured for the
longest PR interval preferably leads I, II, and V1.
n Short PR interval: The PR interval is short when con-
duction of the impulse from atria to ventricles is shorter
than normal (0.12 seconds or 120 milliseconds). This
usually occurs when an accessory pathway or bypass
tract is present connecting the atrium directly to the
ventricle or when conduction of the impulse across the
AV node is enhanced because of a small AV node or
from pharmacologic agents that speed AV nodal con-
duction. This will also occur when there is an ectopic
impulse, meaning that the P wave originates from the
atria or AV junction and not from the sinus node.
PR segment: The PR segment is the isoelectric or flat line
between the P wave and the QRS complex and is measured
from the end of the P wave to the beginning of the QRS com-
plex. It represents the spread of the impulse at the AV node
and His-Purkinje system, with most of the delay occurring at
the level of the AV node. This delay is important so that atrial
and ventricular contraction is coordinated and does not oc-
cur simultaneously. Because the PR segment is isoelectric, it
is used as baseline for measuring the various deflections in
the ECG.
QRS complex: The QRS complex is the next deflection after
the P wave. It represents activation of both ventricles. It is the
Basic Electrocardiography 19
largest complex in the ECG because the ventricles contain
the largest mass of working myocardium in the heart. This is
in contrast to the thinner muscles in the atria, which corre-
sponds to a smaller P wave. The first portion of the ventricle
to be activated is the middle third of the ventricular septum
because the left bundle branch is shorter than the right bun-
dle branch.
Waves of the QRS complex: The QRS complex consists
of the following waves or deflections: Q, R, S, R, S, R,
and S. The use of capital and small letters in identifying
the waves of the QRS complex is arbitrary.
Duration of the QRS complex: The QRS complex is
measured from the beginning of the first deflection, which
may be a Q wave or R wave, to the end of the last deflection.
The width or duration of the QRS complex normally varies
from 0.06 to 0.10 seconds in the adult but may be less in in-
fants and children. The QRS complex corresponds to phase
0 of the transmembrane action potential of a single muscle
cell. Because there are millions of muscle cells in the ven-
tricles that are activated, the total duration of the QRS
complex will depend on how efficiently the whole ventricle
is depolarized. Thus, when there is increased muscle mass
due to hypertrophy of the left ventricle or when there is de-
lay in the spread of the electrical impulse because of bun-
dle branch block or the impulse originates directly from
the ventricles or from a ventricular pacemaker, the dura-
tion of the QRS complex becomes prolonged.
Amplitude: The height of the QRS complex in the limb
leads should measure 5 mm in at least one lead. This in-
cludes the total amplitude above and below the baseline.
In the chest lead, it should measure 10 mm in at least
one lead.
n Low voltage: Low voltage is present when the tallest
QRS complex in any limb lead is 5 mm or the tallest
complex in any chest lead is 10 mm. Low voltage may
be confined only to the limb leads or only to the chest
leads or it may be generalized involving both limb and
chest leads. Low voltage can occur when transmission
of the cardiac impulse to the recording electrode is
diminished because of peripheral edema, ascites,
anasarca, chronic obstructive pulmonary disease (espe-
cially emphysema), obesity, pericardial, or pleural effu-
sion. Low voltage can also occur if the recording elec-
trode is distant from the origin of the impulse.
n Increased voltage: The voltage of the QRS complex
may be increased when there is hypertrophy of the
ventricles. It may be a normal finding in young adults.
Electrical versus mechanical systole: The onset of the
QRS complex marks the beginning of electrical systole,
which is hemodynamically silent. After the ventricles are
depolarized, there is a brief delay before the ventricles
contract causing both mitral and tricuspid valves to close
during systole. Closure of both mitral and tricuspid valves
is audible as the first heart sound (S1), which marks the
beginning of mechanical systole.
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20 Chapter 2
QT interval: The QT interval is measured from the begin-
ning of the QRS complex to the end of the T wave. The
American College of Cardiology/American Heart Associa-
tion/Heart Rhythm Society recommend that the QT interval
should be measured using at least three different leads and
should be the longest QT interval that can be measured in
the 12-lead ECG.
The QT interval is measured from the earliest onset of the
QRS complex to the latest termination of the T wave.
The duration of the QT interval is affected by heart rate.
Thus, the QT interval corrected for heart rate is the QTc.
The QTc is calculated using the Bazett formula: QTc (in
seconds)  QT interval (in seconds)  square root of the
preceding R-R interval (in seconds).
The normal QTc is longer in women than in men. The
QTc interval should not exceed 0.44 seconds (440 milli-
seconds) in women and 0.42 seconds (420 millisec-
onds) in men. A prolonged QT interval is defined as a
QTc 0.44 seconds (440 milliseconds) in men and
0.46 seconds (460 milliseconds) in women and chil-
dren. If bundle branch block or intraventricular
conduction defect of 0.12 seconds is present, the QTc
is prolonged if it measures 0.50 seconds (500 milli-
seconds).
A prolonged QTc interval can be acquired or inherited. It
predisposes to the occurrence of a ventricular arrhythmia
called torsades de pointes. A prolonged QTc, either ac-
quired or inherited, should always be identified because
this subtle abnormality can be lethal.
The difference between the longest and shortest QT inter-
val, when the QT intervals are measured in all leads in a
12-lead ECG, is called QT dispersion. Wide QT dispersion
of 100 milliseconds predicts a patient who is prone to
ventricular arrhythmias.
J Point: The end of the QRS complex and the beginning of
the ST segment is called the J point. The J point marks the
end of depolarization and the beginning of repolarization of
the transmembrane action potential.
J point elevation: J point elevation is frequently seen in
normal patients and can be attributed to the difference in
repolarization between the endocardial and epicardial
from
cells. The ventricular epicardium exhibits a spike and
dome configuration during phases 1 and 2 of the action
potential that is not present in the endocardium. This
difference in potential during early repolarization causes
. The male and female patterns
current to flow between the endocardium and epi-
cardium. This current is recorded as elevation of the J
point in the surface ECG. The difference in repolariza-
tion becomes even more pronounced in the setting of hy-
pothermia or hypercalcemia. When the J point becomes
very prominent, it is often called a J wave or Osborn
wave.
ST segment: The ST segment is the interval between the end
of the QRS complex and the beginning of the T wave. This cor-
responds to the plateau (phase 2) of the transmembrane
action potential. During phase 2, the transmembrane poten-
tial of the ventricular myocardial cells remains constant at 0
mV for a relatively long period. Thus, the ST segment re-
mains isoelectric and at the same baseline level as the PR and
TP segments. An ST segment is considered abnormal when it
deviates above or below this baseline by 1 mm. The ST seg-
ment is also abnormal when there is a change in its morphol-
ogy such as when it becomes concave or convex or has an up-
sloping or downsloping configuration. Contraction of the
ventricular myocardium is sustained due to entry of calcium
into the cell, which triggers the release of more calcium from
intracellular storage sites, namely the sarcoplasmic reticu-
lum. During this period, the ventricles are absolutely refrac-
tory to any stimuli.
ST elevation in normal individuals: Elevation of
the ST segment is often seen in normal healthy individu-
als especially in men. In one study, 91% of 6014 normal
healthy men in the US Air Force aged 16 to 58 had 1 to 3
mm of ST segment elevation. ST elevation therefore is an
expected normal finding in men.
n The ST elevation in normal healthy males is com-
monly seen in a younger age group especially among
African American men. The prevalence declines grad-
ually with age. In one study, ST elevation of at least
1 mm was present in 93% of men aged 17 to 24 years,
but in only 30% by age 76 years. In contrast, women
less commonly demonstrate ST elevation, and its
presence is not age related. In the same study, approx-
imately 20% of women had ST elevation of at least
1 mm and there was no age predilection.
n ST segment elevation in normal healthy individuals
was most often seen in precordial leads V1 to V4 and
was most marked in V2. The morphology of the nor-
mal ST elevation is concave.
n The ST segment elevation in men is much more pro-
nounced than that noted in women with most of the
men having ST elevation of 1 mm. Most women
have ST elevation measuring 1 mm. Thus, ST eleva-
tion of 1 mm has been designated as a female pat-
tern and ST elevation of at least 1 mm associated with
a sharp take-off of the ST segment of at least 20
baseline, has been designated as a male pattern. The
pattern is indeterminate if ST elevation of at least
1 mm is present but the takeoff of the ST segment
from baseline is 20
can be visually recognized without making any meas-
urements in most normal ECGs.
n Another pattern of ST segment elevation seen in nor-
mal healthy individuals is one associated with early re-
polarization. This type of ST elevation is often accom-
panied by a J wave at the terminal end of the QRS
complex. The ST elevation is most frequently seen in
V4 and is frequently accompanied by tall and peaked T
waves (see Chapter 23, Acute Coronary Syndrome: ST
Elevation Myocardial Infarction).
LWBK271-C02_09-22.qxd 1/29/09 1:51 PM Page 21 LWBK271-C01_01-08.qxd
n Another ST elevation considered normal variant is the
presence of ST elevation accompanied by inversion of
the T wave in precordial leads V3 to V5.
Abnormal ST elevation: Abnormal causes of ST eleva-
tion include acute myocardial infarction, coronary va-
sospasm, acute pericarditis, ventricular aneurysm, left
ventricular hypertrophy, hyperkalemia, left bundle
branch block, and the Brugada syndrome. This is further
discussed in Chapter 23, Acute Coronary Syndrome: ST
Elevation Myocardial Infarction.
T wave: The T wave corresponds to phase 3 of the trans-
membrane action potential and represents rapid repolariza-
tion. The different layers of the myocardium exhibit different
repolarization characteristics.
Repolarization of the myocardium normally starts from
epicardium to endocardium because the action potential
duration of epicardial cells is shorter than the other cells
in the myocardium. Thus, the onset of the T wave repre-
sents the beginning of repolarization of the epicardium
and the top of the T wave corresponds to the complete re-
polarization of the epicardium.
Repolarization of the endocardium takes longer than re-
polarization of the epicardium. Therefore, the repolariza-
tion of the endocardium is completed slightly later at the
downslope of the T wave.
In addition to the endocardial and epicardial cells, there
is also a population of M cells constituting 30% to 40%
of the mid-myocardium. The M cells have different elec-
trophysiologic properties with repolarization taking
even longer than that seen in epicardial and endocardial
cells. M cell repolarization consequently corresponds to
the end of the T wave.
The duration and amplitude of the T wave is variable, al-
though, generally, the direction (axis) of the T wave in
the 12-lead ECG follows the direction of the QRS com-
plex. Thus, when the R wave is tall, the T wave is upright,
and when the R wave is smaller than the size of the S
wave, the T wave is inverted.
The shape of the normal T wave is rounded and smooth
and slightly asymmetric with the upstroke inscribed slowly
and the downslope more steeply. The T wave is considered
abnormal if the shape becomes peaked, notched, or dis-
torted or if the amplitude is increased to more than 5 mm
in the limb leads and 10 mm in the precordial leads. It is
also abnormal when the T wave becomes symmetrical or
inverted. This is further discussed in Chapter 24 (Acute
Coronary Syndrome: Non-ST Elevation Myocardial Infarc-
tion and Unstable Angina).
At bedside, the end of the T wave coincides with the clo-
sure of the aortic and pulmonic valves. This is audible as
S2 during auscultation. The aortic second heart sound
therefore can be used for timing purposes to identify the
end of left ventricular systole and beginning of diastole.
Any event before the onset of S2 is systolic and any event
occurring after S2 (but before the next S1) is diastolic.
Basic Electrocardiography 21
TQ interval: The TQ interval is measured from the end of
the T wave to the onset of the next QRS complex. It corre-
sponds to phase 4 of the transmembrane action potential.
The T-P or TQ segment is used as the isoelectric baseline for
measuring deviations of the J point or ST segment (eleva-
tion or depression) because the transmembrane action po-
tential is at baseline and there is no ongoing electrical activ-
ity at this time. Thus, the TQ segment is not affected by
other waves. However, if there is sinus tachycardia and the
PR interval is markedly prolonged and the P wave is in-
scribed at the end of the T wave, then the long PR segment
is used as an alternate baseline for measuring deviations of
the J point or ST segment.
T-P segment: The T-P segment is a subportion of the
TQ interval, which represents the interval between the
end of ventricular repolarization (end of T wave) and the
onset of the next sinus impulse (P wave). It marks the end
of the previous cycle and the start of the next cardiac cy-
cle beginning with the sinus impulse. This segment usu-
ally serves as baseline for measuring deviations of the J
point or ST segment.
At bedside, diastole starts with the closure of the aortic and
pulmonic valves (audible as the second heart sound S2) and
continues until the closure of the mitral and tricuspid valves
(audible as the first heart sound S1). This closely corresponds
to the TQ interval in the ECG.
The U wave: Although a U wave may be seen as another de-
flection after the T wave, this is not consistently present. U
waves are commonly visible when the heart rate is slow (usu-
ally 65 bpm) and are rarely recorded with heart rates above
95 bpm. U waves are best recorded in the anterior precordial
leads due to the proximity of these leads to the ventricular
myocardium. Repolarization of the His-Purkinje system co-
incides with the inscription of the U wave in the ECG and is
more delayed than the repolarization of the M cells. The U
wave therefore is most probably because of repolarization of
the His-Purkinje system.
The U wave follows the direction of the T wave and QRS
complex. Thus, the U wave is upright when the T wave is
upright. When the U wave is inverted or prominent, it is
considered pathologic.
An abnormal U wave indicates the presence of myocardial
disease or electrolyte abnormality. Prominent U waves
may be due to hypokalemia or drugs such as quinidine.
Inversion of the U wave is always pathologic and is most
commonly due to myocardial ischemia, hypertension, or
valvular regurgitation. Its presence may be transient or it
may be more persistent.
Abnormal waves: The delta wave, epsilon wave, and Os-
born wave are other waves in the ECG that should be recog-
nized because these waves are pathologic. J. Willis Hurst
traced the historical origin of these waves as follows:
Delta wave: The slow, slurred upstroke of the QRS
complex, associated with the Wolff-Parkinson-White syn-
drome, is due to premature excitation of the ventricle
LWBK271-C02_09-22.qxd 1/29/09 1:51 PM Page 22 LWBK271-C01_01-08.qxd
22 Chapter 2
because of the presence of an accessory pathway connect-
ing the atrium directly to the ventricle. This early deflec-
tion of the QRS complex is called the delta wave because
it resembles the shape of a triangle () which is the sym-
bol of the Greek capital letter delta. (Note that the slow
slurred upslope of the initial QRS complex resembles the
left side of the triangle.)
Epsilon wave: The epsilon wave is associated with right
ventricular dysplasia and represents late activation of the
right ventricular free wall. This is represented as a small de-
flection at the end of the QRS complex and is best recorded
in leads V1 to V3. Epsilon comes next to the Greek letter
delta. The delta wave occurs at the beginning of the QRS
complex (because of early activation of the ventricle and is a
preexcitation wave), whereas the epsilon wave occurs at the
end of the QRS complex (because of late activation of the
free wall of the right ventricle and is a postexcitation wave).
Osborn wave: When the J point is exaggerated, it is
called J wave. The wave is named after Osborn, who de-
scribed the association of this wave to hypothermia.
Suggested Readings
Antzelevitch C. The M Cell. J Cardiovasc Pharmacol Ther.
1997;2:7376.
Ariyarajah V, Frisella ME, Spodick DH. Reevaluation of the cri-
terion for interatrial block. Am J Cardiol. 2006;98:936937.
Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006
key data elements and definitions for electrophysiology stud-
ies and procedures: a report of the American College of Car-
diology/American Heart Association Task Force on Clinical
Data Standards (ACC/AHA/HRS Writing Committee to
Develop Data Standards on Electrophysiology). J Am Coll
Cardiol. 2006;48:23602396.
Correale E, Battista R, Ricciardiello V, et al. The negative U wave:
a pathogenetic enigma but a useful often overlooked bedside
diagnostic and prognostic clue in ischemic heart disease.
Clin Cardiol. 2004;27:674677.
Dunn MI, Lipman BS. Basic physiologic principles. In: Lipman-
Massie Clinical Electrocardiography. 8th ed. Chicago: Year-
book Medical Publishers, Inc; 1989:2450.
Hurst JW. Naming of the waves in the ECG, with a brief account
of their genesis. Circulation. 1998;98:19371942.
Marriott HJL. Complexes and intervals. In: Practical Electrocar-
diography. 5th ed. Baltimore: Williams and Wilkins; 1972:
1633.
Moss AJ. Long QT syndrome. JAMA. 2003;289:20412044.
Phoon CKL. Mathematic validation of a shorthand rule for cal-
culating QTc. Am J Cardiol. 1998;82:400402.
Sgarbossa EB, Wagner GS. Electrocardiography. In: Textbook of
Cardiovascular Medicine. 2nd ed. Editor is Topol EJ Philadel-
phia: Lippincott-Williams and Wilkins; 2002:13301383.
Surawicz B. U waves: facts, hypothesis, misconceptions and mis-
nomers. J Cardiovasc Electrophysiol. 1998;9:11171128.
Surawicz B, Parikh SR. Prevalence of male and female patterns
of early ventricular repolarization in the normal ECG of
males and females from childhood to old age. J Am Coll Car-
diol. 2002;40:18701876.
Yan GX, Antzelevitch C. Cellular basis for the normal T wave
and the electrocardiographic manifestations of the long-QT
syndrome. Circulation. 1998;98:19281936.
Yan GX, Lankipalli RS, Burke JF, et al. Ventricular repolarization
components of the electrocardiogram, cellular basis and
clinical significance. J Am Coll Cardiol. 2003;42:401409.
Yan GX, Shimizu W, Antzelevitch C. Characteristics and distri-
bution of M cells in arterially perfused canine left ventricular
wedge preparations. Circulation. 1998;98:19211927.
LWBK271-C03_23-29.qxd 29/1/09 8:44 pm Page 23 LWBK270-4119G-C02_073-110.qxd

3
The Lead System

Basic Principles Bipolar Leads I, II, and III

The electrical impulses originating from the heart can
be transmitted to the body surface because the body
contains fluids and chemicals that can conduct electric-
ity. These electrical impulses can be recorded by placing
electrodes to the different areas of the body. Thus, if a
left arm electrode is connected to the positive pole of a
galvanometer and a right arm electrode is connected to
the negative pole, the magnitude as well as the direction
of the electrical impulse can be measured.
Any flow of current directed toward the positive
(left arm) electrode is conventionally recorded as an
upright deflection (Fig. 3.1A).
Any flow of current away from the positive electrode
is recorded as a downward deflection (Fig. 3.1B).
The height of the electrocardiogram (ECG) deflec-
tion represents the difference in potential between
the two electrodes.
Bipolar Leads: An imaginary line connecting any
two electrodes is called a lead. A lead is bipolar when
both positive and negative electrodes contribute to
the deflection in the ECG. The positive and negative
electrodes are placed at an equal distance away from
the heart and the resulting ECG deflection is the
sum of the electrical forces going in opposite direc-
tions. Leads I, II, and III are examples of bipolar
leads.
Lead I: Lead I is conventionally constructed such
that the left arm electrode is attached to the positive
pole of the galvanometer and the right arm to the
negative pole (Fig. 3.2A). If the direction of the im-
pulse is toward the left arm, an upward or positive
deflection is recorded. If the direction of the im-
pulse is toward the right arm, a negative or down-
ward deflection is recorded.

B A downward deflection is Figure 3.1: Lead. The direction and

recorded if the flow of current
magnitude of the electrical impulse can be
is away from the positive
electrode measured with a galvanometer (G). The left
arm electrode is conventionally attached to
An upward deflection is the positive pole of the galvanometer and
A recorded if the flow of current is the right arm electrode to the negative
toward the positive electrode pole. An imaginary line connecting the two
electrodes is called a lead. Any flow of cur-
Negative rent directed toward the positive electrode
Positive Electrode
Electrode R L (Left Arm) will be recorded as an upright deflection
(Right Arm)
(A). Any current moving away from the
positive electrode is recorded as a
Lead
downward deflection (B).

Galvanometer
- G
+

23
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24 Chapter 3

Lead I Lead II Lead III

Figure 3.2: Bipolar Leads I, II,
and III. AC represent the location of
the electrodes for leads I, II, and III, re- - I + - -
spectively. Any flow of current toward
the positive electrode will record a
II III
positive deflection. The imaginary line
connecting the two electrodes is the A B C
ECG lead. + +

Lead II: The left leg is attached to the positive pole
and the right arm to the negative pole (Fig. 3.2B).
When the direction of the impulse is toward the left
leg, a positive deflection is recorded. When the di-
rection of the impulse is toward the right arm, a
downward deflection is recorded.
Lead III: The left leg is attached to the positive pole
and the left arm to the negative pole (Fig. 3.2C).
When the direction of the impulse is toward the left
leg, an upward deflection is recorded. When the di-
rection of the impulse is toward the left arm, a
downward deflection is recorded.
Lead I transects an imaginary line from one shoulder
to the other shoulder and represents an axis of 0 to
180 (Fig. 3.3A).
Lead II transects an imaginary line between the left leg
and right arm and represents an axis of 60 to 120
(Fig. 3.3B).
Lead III transects an imaginary line between the left leg
and the left arm and represents an axis of 120 and
60 (Fig. 3.3C).
Leads I, II, and III can be arranged to form the
Einthoven triangle (Fig. 3.3D, E) as shown. The leads
can also be superimposed on each other by combining
all three leads at their mid-points to form a triaxial
reference system representing the frontal plane of the
body (Fig. 3.3F).
Unipolar Leads: When one electrode is capable of de-
tecting an electrical potential (exploring electrode) and
the other electrode is placed at a distant location so that
it will not be affected by the electrical field (indifferent
electrode), the lead that is created is a unipolar lead. A
unipolar lead therefore has only one electrode that con-
tributes to the deflection in the ECG. The other electrode
serves as a ground electrode and is theoretically neutral.
The exploring electrode: Only the exploring elec-
trode is capable of measuring the flow of current.
This electrode is connected to the positive pole of
the galvanometer. If the flow of current is directed
toward the exploring electrode, an upward deflec-
tion is recorded. If the flow of current is away from
the exploring electrode, a downward deflection is
recorded. The exploring electrodes of the three
unipolar limb leads are conventionally placed in the
right arm, left arm and left foot and were originally
called VR, VL, and VF respectively.
The ground electrode: The ground electrode is
constructed by placing a resistance of 5,000 ohms to
each of the three limb electrodes and connecting
them together to form a central terminal (Fig. 3.4).

Figure 3.3: Bipolar Leads I, II, and Lead I (0 to 180 0) Lead II (+60 to -1200 ) Lead III (+120 to - 600)
III. A, B, and C represent leads I, II, and --1200 - 600
III, respectively. The leads form an - I + -
0 0
Einthoven triangle (D, E), which can be 180 0
rearranged to form a triaxial reference II III
system by combining all three leads at
A B + C +
each midpoint as shown (F). +60
0
+120

-1200 0

- I + - Lead I + - -- 60
- - - - - +
1800 I 00
II III Lead II Lead III

D + F + +II
+ E + + III
+600
+1200
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The Lead System 25

Central Terminal Ground Electrode

- +
G

Exploring
R Electrode

L
5000-Ohm
F
Resistance

Figure 3.4: Unipolar Leads VR, VL, and VF. Diagram shows the original con-
struction of the unipolar limb leads VR, VL, and VF. Each limb lead is connected to a
resistance of 5,000 ohms to form a central terminal. The central terminal serves as
the ground electrode and is connected to the negative pole of the galvanometer.
The exploring electrode, which in this example is in the left foot, is connected to the
positive pole. R, right arm; L, left arm; F, left foot.

The central terminal is connected to the negative
pole of the galvanometer. This serves as the ground
electrode, which has a potential of zero or near zero.
Augmented Unipolar Leads
AVR, AVL, and AVF
Augmented unipolar leads aVR, aVL, and aVF:
When the exploring electrode was disconnected from
the central terminal, the size of the ECG deflection in-
creased by 50%. Thus, the augmented unipolar leads
VR, VL, and VF were renamed aVR, aVL, and aVF and
became the standard unipolar limb leads.
Lead aVR: The unipolar electrode is positioned
over the right arm and is capable of detecting the
flow of electrical impulse directed toward the right
shoulder. The location of aVR is 150 (Fig. 3.5A).
Lead aVL: The unipolar electrode is positioned over
the left arm and is capable of detecting potentials

-1500 - 300
+ +
aVR aVL

+ 0
+90 aVF
A B C

Ground
Central Electrode
Terminal
+ + +
G G G

R R R
L Exploring L L
Electrode
F F F

aVR aVL aVF

Figure 3.5: Augmented Unipolar Leads aVR, aVL, and aVF. The upper panel shows the position of the
exploring electrode for leads aVR, aVL, and aVF. The lower panel shows the connection of the exploring electrode
and the central terminal. R, right arm; L, left arm; F, left foot.
LWBK271-C03_23-29.qxd 29/1/09 8:44 pm Page 26 LWBK270-4119G-C02_073-110.qxd

26 Chapter 3

directed toward the left shoulder. The location of
aVL is 30 (Fig. 3.5B).
Lead aVF: The unipolar electrode is positioned over
the left leg and is capable of detecting potentials di-
rected toward the left groin. The location of aVF is
90 (Fig. 3.5C).
Unipolar Leads AVR, AVL, and AVF
The three augmented unipolar leads aVR, aVL, and
aVF (Fig. 3.6A), and the three standard bipolar leads I,
II, and III (Fig. 3.6B) complete the six leads represent-
ing the frontal plane of the body. These six leads can be
rearranged to form a hexaxial reference system as
shown (Fig. 3.6C). All unipolar leads are identified
with a letter V.
The location of each lead as well as the position of the
positive and negative terminals of each lead is crucial in
understanding the 12-lead ECG.
The Precordial Leads
Precordial leads: Six precordial leads were later added
to the six frontal leads to complete the 12-lead ECG. All
six precordial leads are unipolar and are identified with
a letter V. When the lead is unipolar, only the exploring
electrode contributes to the generation of the electrical
complex.
Exploring electrode: The location of the exploring
electrodes in the chest is universally standardized.
The electrodes are labeled V1 to V6. The standard
universal position of V1 to V6 are as follows:
n V1 is located at the 4th intercostal space immedi-
ately to the right of the sternum.
n V2 is located at the 4th intercostal space immedi-
ately to the left of the sternum.
n V3 is located between V2 and V4.
n V4 is located at the 5th intercostal space, left mid-
clavicular line.
n V5 is located at the same horizontal level as V4,
left anterior axillary line.
n V6 is located at the same level as V5, left mid axil-
lary line.
Ground electrode: The ground electrode is the
central terminal similar to Figure 3.4 and is con-
structed by placing a resistance of 5,000 ohms to
each of the three limb electrodes (Fig. 3.7). The cen-
tral terminal is connected to the negative pole of the
galvanometer and serves as the ground electrode,
which has a potential of zero.

0
Figure 3.6: Hexaxial Reference Sys- - 150 aVR 0
- 30
tem Representing the Frontal
aVR - I + aVL - Lead I + aVL
Plane. The standard bipolar leads I, II,
and III and the augmented unipolar limb
- - -
- -
leads aVR, aVL, and aVF make up the hexa-
xial reference system representing the II Lead II Lead III
III
frontal plane. (A) The location of these
leads in relation to the body. (B, C) How
these six leads are related to each other. + + + +
0
+ 90
A aVF B aVF

0
- 900
-120 - - 600
- aVL
aVR - - 300
0
- 150 +
+

+1800 - + 0
0
I

- -
+1500 + 300
+ +
+1200 + +600
0
+ 90 II
III
C aVF
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The Lead System 27

Central Terminal Ground Electrode Figure 3.7: The Precordial Leads. The
construction of the unipolar chest leads is shown dia-
- + grammatically. The precordial electrode is the explor-
G
V1 V2-V6 ing electrode. Six exploring electrodes are positioned
in V1 to V6.The ground electrode consists of three
R limb electrodes individually attached to a 5,000-
ohm resistance and connected together to form a
L central terminal. R, right arm; L, left arm; F, left foot.
Exploring Chest
5000-Ohm
Resistance
F Electrode

The latest recommendations of the American Heart Associa-

The 12-Lead ECG tion regarding the ECG include the following:
Until further studies are available, the extremity elec-
The six frontal or limb leads and the six horizontal or trodes are placed distal to the shoulders and hips and not
precordial leads complete the 12-lead ECG (Fig. 3.8A, B). necessarily at the wrists or ankles. This reduces motion
artifacts and ECG voltage and duration are less affected
than if the leads are placed more distally.
Standard and Special Leads All leads in the standard 12-lead ECG are effectively bipo-
lar. This is based on the principle that all leads consist of
an electrode that is paired to another electrode. This in-
Standard 12-lead ECG: The 12-lead ECG is recorded
cludes the standard limb leads as well as the leads where
with the patient supine and a pillow supporting the head. the exploring electrode is paired with an indifferent elec-
trode consisting of the central terminal or its modifica-
tion. Thus, standard leads I, II, and III; augmented limb
A: Frontal Plane Superior
leads aVR, aVL, and aVF; and the six precordial leads V1
- 900
-1200 - - 600 aVL to V6 are all effectively bipolar and the use of bipolar and
aVR - - - 300 unipolar to describe these leads is discouraged.
- 1500 +
Misplacement of the precordial leads is a common cause
+
of variability in the ECG, especially when serial tracings
Right +1800 - + 0
0
I Left are being interpreted. The position of V4 should be fol-
lowed horizontally; thus, V5 and V6 should be in the same
- - + 300
+1500 horizontal position as V4 rather than at a lower position if
+ + the course of the 5th intercostal space is followed laterally.
+1200 + +600
+ 90 0 In women, it is recommended that the precordial elec-
III II
aVF trodes should be placed under rather than over the breast,
Inferior thus allowing V5 and V6 to follow the horizontal position
of V4. If the anterior axillary line is not well defined, V5 is
B: Horizontal Plane Posterior
positioned midway between V4 and V6. The position of V1
and V2 is at the 4th intercostal space at the right and left
sternal borders respectively. When V1 and V2 are erro-
Right V6 Left neously placed higher at the 2nd intercostal space, the fol-
lowing changes may occur:
V5
V4 n A smaller r wave is recorded from V1 to V3. The R wave
V1 V2 V3
reduction is approximately 1 mm per interspace, caus-
Anterior
ing poor R wave progression, which can be mistaken
for anterior myocardial infarction (MI).
n Terminal r waves with T wave inversion resulting in
rSr pattern in V1 and V2 are recorded similar to the
configuration in lead aVR.
V1 V2 V3 V4 V5 V6
n If the diaphragm is displaced downward and the heart
Figure 3.8: The 12-Lead Electrocardiogram. (A) The po- becomes vertically oriented, as when there is chronic
sition of the six limb leads in the frontal plane. (B) The six obstructive lung disease, the normal location of V3
precordial leads in the horizontal plane. and V4 will place these leads in a relatively higher
LWBK271-C03_23-29.qxd 29/1/09 8:44 pm Page 28 LWBK270-4119G-C02_073-110.qxd
28 Chapter 3
position than the ventricles; thus, deep S waves will be
recorded in these leads, which can be mistaken for an-
terior MI.
Finally, when the extremity leads are modified so that the
leads are placed in the torso rather than the extremities,
the ECG is not considered equivalent to the standard
ECG. Similarly, tracings obtained in the sitting or upright
position is not equivalent to the standard ECG, which is
recorded supine.
It has also been observed that when V1 and V2 are placed
higher than their normal location, small q waves may be
recorded in V2 and V3, especially in the presence of left an-
terior fascicular block.
Special Electrodes: In addition to the 12 standard ECG
leads, special leads can be created by repositioning some elec-
trodes to the different areas on the chest.
Special leads V7,V8, and V9: V7 is located at the left pos-
terior axillary line at the same level as V6. V8 is located just
below the angle of the left scapula at the same level as V7
and V9 just lateral to the spine at the same level as V8.
These leads supplement the 12-lead ECG in the diagnosis
of posterolateral ST elevation MI and should be recorded
when reciprocal ST segment depression is present in V1 to
V3.
Right sided precordial leads V3R, V4R, V5R, and V6R:
After recording the usual standard 12-lead ECG, special
leads V3R, V4R, V5R, and V6R can be added by moving
precordial leads V3, V4, V5, and V6 to the right side of the
chest corresponding to the same location as that on the
left. These leads are very useful in the diagnosis of right
ventricular MI, dextrocardia, and right ventricular hyper-
trophy. These leads should be recorded routinely when
there is acute coronary syndrome with ST elevation MI
involving the inferior wall (leads II, III, and aVF).
Other lead placement used for detection of
arrhythmias:
n CF, CL, and CR leads: Bipolar leads have electrodes
positioned in the arms or leg, which are equidistant
from the heart. When one electrode is moved to the
precordium and the other electrode is retained in its
original position in the arm or leg, the chest electrode
will contribute more to the recording than the remote
electrode.
n Thus, a CL lead is created if one electrode is placed on
the chest and the more remote electrode is retained in
its original position in the left arm. If the chest elec-
trode is placed in V1 and the remote electrode is at the
left arm, the lead is identified as CL1.
n CR lead is created when the remote electrode is re-
tained in the right arm. If the chest electrode is placed
in V1 and the remote electrode is at the right arm, the
lead is identified as CR1.
n CF lead is created when the remote electrode is re-
tained in the left foot. If the chest electrode is placed in
V1 and the remote electrode is at the left foot, the lead
is identified as CF1.
n Modified CL1 or MCL1: MCL1 is a lead that resembles
V1. The lead is bipolar and is a modified CL1 lead. The
positive electrode is placed at V1 and the negative elec-
trode is placed close to the left shoulder. A ground
electrode is placed at the other shoulder. It is fre-
quently used for detecting arrhythmias during contin-
uous monitoring of patients admitted to the coronary
care unit.
n Lewis lead: When the P wave is difficult to recognize,
the right arm electrode is moved to the 2nd right in-
tercostal space just beside the sternum and the left
arm electrode to the 4th right intercostal space also
beside the sternum. Lead I is used for recording.
n Fontaine lead: The Fontaine leads are special leads for
recording epsilon waves in patients with arrhythmo-
genic right ventricular dysplasia. The epsilon waves are
usually difficult to record using only the standard 12
leads. The right arm electrode is placed at the
manubrium and the left arm electrode at the xiphoid.
Additionally, the left foot electrode may be moved to
position V4. Leads I, II, and III are used for recording.
n Other modifications: Other special leads can be cre-
ated if the P waves cannot be visualized by placing the
right arm electrode at V1 position and the left arm
electrode anywhere to the left of the sternum or more
posteriorly at V7 position. Lead I is recorded.
n Esophageal and intracardiac electrodes: These elec-
trodes can be connected to any precordial or V lead,
usually V1, for recording atrial activity (P waves) if the
P wave cannot be visualized in the surface ECG.
n A pill electrode can be swallowed and positioned
behind the left atrium in the esophagus and con-
nected to a precordial lead usually V1. The ECG is
recorded in V1.
n An electrode can also be inserted transvenously and
positioned into the right atrium. The electrode is
connected to a precordial lead and recorded as above.
n A central venous catheter, which is often already in
place for intravenous administration of medica-
tions, is filled with saline. A syringe needle is in-
serted to the injecting port of the central line and at-
tached with an alligator clamp to a precordial lead,
usually V1. The ECG is recorded in V1. This special
lead is for recording atrial activity if the P waves are
not visible in the surface ECG.
Suggested Readings
Burch GE, Winsor T. Principles of electrocardiography. In: A
Primer of Electrocardiography, 5th ed. Philadelphia: Lea and
Febiger; 1966;1766.
LWBK271-C03_23-29.qxd 29/1/09 8:44 pm Page 29 LWBK270-4119G-C02_073-110.qxd
Burch GE, Winsor T. Precordial leads. In: A Primer of Electrocar-
diography, 5th ed. Philadelphia: Lea and Febiger; 1966;146184.
Dunn MI, Lippman BS. Basic ECG principles. In: Lippman-
Massie Clinical Electrocardiography, 8th ed. Chicago: Year-
book Medical Publishers; 1989:5162.
Hurst JW. Naming of the waves in the ECG, with a brief account
of their genesis. Circulation. 1998;19371942.
Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the
standardization and interpretation of the electrocardiogram:
part I: the electrocardiogram and its technology: a scientific
statement from the American Heart Association Electrocar-
diography and Arrhythmias Committee, Council on Clinical
The Lead System 29
Cardiology; the American College of Cardiology Founda-
tion; and the Heart Rhythm Society. J Am Coll Cardiol.
2007;49:11091127.
Madias JE, Narayan V, Attari M. Detection of P waves via a
saline-filled central venous catheter electrocardiographic
lead in patients with low electrocardiographic voltage due
to anasarca. Am J Cardiol. 2003;91:910914.
Marriott HJL. Chapter 4. Electrical Axis. In: Practical Electrocardio-
graphy, 5th ed. Baltimore: Willliams & Wilkins; 1972:3443.
Wagner GS. Cardiac electrical activity and recording the electro-
cardiogram. In: Marriotts Practical Electrocardiography, 10th
ed. Philadelphia: Lippincott Williams and Wilkins; 2001;241.
LWBK271-C04_30-47.qxd 1/30/09 11:22 AM Page 30 Aptara Inc.

4
The Electrical Axis and
Cardiac Rotation
the heart may be normal or it may be rotated clock-
The Frontal and Horizontal Planes wise or counterclockwise.

Figuring the direction or axis of the QRS complex (or

any wave in the electrocardiogram [ECG]) requires a
thorough understanding of the location of each of the
different leads in the 12-lead ECG. This knowledge is
crucial and provides the basic foundation for under-
standing electrocardiography. Before attempting to
read this chapter, a review of the previous chapter is
mandatory.
The ECG mirrors both frontal and horizontal planes of
the body and is thus tridimensional.
Frontal plane: The frontal plane is represented by
leads I, II, III, aVR, aVL, and aVF. It includes the
left/right and superior/inferior orientation of the
body (Fig. 4.1A). The electrical position of the heart
in the frontal plane is described as axis deviation.
Thus, the axis of the QRS complex may be normal
or it may be deviated to the left, to the right or to the
northwest quadrant.
Horizontal plane: The horizontal plane is repre-
sented by leads V1 to V6 (Fig. 4.1B). It includes
left/right and anteroposterior orientation of the
body. The position of the heart in the horizontal
plane is described as rotation. Thus, the rotation of
The Frontal Plane
Frontal plane: Using the hexaxial reference system
(Fig. 4.2), the frontal plane can be divided into four
quadrants.
Normal quadrant: The left lower quadrant be-
tween 0 and 90 represents normal quadrant.
Left upper quadrant: The left upper quadrant be-
tween 0 and 90 represents left axis deviation.
Right lower quadrant: The right lower quadrant
between 90 and 180 represents right axis devi-
ation.
Right upper quadrant: The quadrant between
90 and 180 is either extreme right or extreme
left axis deviation. Often, it is not possible to differ-
entiate whether the axis has deviated extremely to
the right or extremely to the left; thus, this axis is of-
ten called northwest axis.
Normal axis: The normal QRS axis depends on the age
of the patient.

Figure 4.1:The 12-Lead Superior

Electrocardiogram. The lo- - 900 Posterior
cation of the different leads in
-
the frontal (A) and horizontal Northwest Left
(B) planes is shown. Axis Axis Right Left
Right 1800 - + 00 I Left V6 00
Right Normal
Axis Axis V5
300
V4
V1 V2 V 3 0
0 60
1200 900 75
+
+ 900
A aVF B
Inferior Anterior

30
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The Electrical Axis and Cardiac Rotation 31

SUP
ever, because the normal axis extends up to 30, an
- axis of 1 to 30 is considered part of the normal
-1200 0
90 - 600 axis (Fig. 4.2).
-1500 - 300
aVR Northwest aVL
Axis LAD
0
Figuring Out the Electrical Axis
R + 1800 I 0 L
Normal
RAD Quadrant Basic considerations: Before attempting to deter-
+ 1500 + 300
mine the axis of any deflection in the ECG, the location
Normal Axis of all the six leads in the frontal plane as well as the lo-
0
III0 II -30 to +90
+ 120 aVF + 600 cation of the positive and negative terminals of each
+90 lead should be mastered. The ECG deflection is maxi-
INF mally upright if the flow of current is directed toward
the positive side of the lead and is maximally inverted if
Figure 4.2: The Frontal Plane and the Hexaxial Refer- the flow of current is directed toward the negative side.
ence System. The frontal plane is represented by the six limb Thus, if the flow of current is parallel to lead I (0 to
leads. The position of the limb leads and the location of the dif- 180), lead I will record the tallest deflection if the flow
ferent quadrants in the frontal plane are shown. Note that the of current is directed toward 0 and the deepest deflec-
leads are 30 apart. The normal axis in the adult extends from tion if the flow of current is directed toward 180 (Fig.
30 to 90, thus 1 to 30 is considered normal axis. LAD, 4.3A, B).
left axis deviation; RAD, right axis deviation; L, left; R, right; SUP, The lead perpendicular to lead I will record an iso-
superior; INF, inferior. electric complex. Isoelectric or equiphasic implies
that the deflection above and below the baseline are
about equal. Since lead aVF is perpendicular to lead
I, lead aVF will record an isoelectric deflection (Fig.
4.3C, D).
In newborns up to 6 months of age, the normal QRS Determining the electrical axis: The electrical axis
axis is 90 (vertical axis). With increasing age, or direction of the QRS complex (or any wave in the
the axis moves horizontally leftward toward 0. It is ECG) can be determined by several methods. Although
rare in children to have a horizontal axis. the area under the QRS complex provides a more accu-
In adults, the normal axis extends horizontally from rate electrical axis, the area is not readily measurable.
90 to 30. The axis 1 to 30 is located in the For convenience, the amplitude of the QRS complex is
left upper quadrant and is left axis deviation. How- measured instead.

Figure 4.3: Leads I and aVF.

0 - + 00 0 - + 00 Lead I and aVF are perpendicular
180 180 I
I to each other. The electrocardio-
A B gram deflection in lead I will reg-
ister the tallest deflection if the
current is directed toward the
0 0
-90 -90 positive electrode (0) as shown
in A. It will record the deepest
deflection if the current is
directed toward 180 or the neg-
180
0 - + 00 180
0 - + 00 ative electrode as shown in B.
I I
The lead perpendicular to lead I
will record an isoelectric deflec-
tion. Because aVF is perpendicu-
+90
0
+90
0 lar to lead I, aVF will record an
aVF aVF isoelectric complex (C, D).

or or
C D
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32 Chapter 4
Figure 4.4: Perpendicular Leads I and aVF
0 0
Leads. In the frontal plane, the - 90
following leads are perpendicular
to each other: Leads I and aVF (A),
Leads II and aVL (B) and lead III 0
180
and aVR (C).
aVF
A + 90
0 B
Method 1: Look for an isoelectric complex: When an
isoelectric QRS complex is present in any lead in the
frontal plane, the axis of the QRS complex is perpendicu-
lar to the lead with the isoelectric complex. The following
leads in the frontal plane are perpendicular to each other.
Lead I is perpendicular to lead aVF (Fig. 4.4A).
n When an equiphasic QRS complex is recorded in
lead I (0), the axis of the QRS complex is 90
or 90.
n Similarly, when an equiphasic QRS complex is
recorded in lead aVF (+90), the axis of the QRS
complex is 0 or 180.
Lead II is perpendicular to lead aVL (Fig. 4.4B).
n When an equiphasic QRS complex is recorded in
lead II (+60), the axis of the QRS complex is
30 or 150.
n Similarly, when an equiphasic QRS complex is
recorded in lead aVL (30), the axis of the QRS
complex is 60 or 120.
Lead III is perpendicular to lead aVR (Fig. 4.4C).
n When an equiphasic QRS complex is recorded in
lead III (120), the axis of the QRS complex is
150 or 30.
n Similarly, when an equiphasic QRS complex is
recorded in lead aVR (150), the axis of the
QRS complex is 120 or 60.
Figuring Out the Electrical Axis
when an Equiphasic Complex is
Present
Lead I is equiphasic: If the QRS complex in lead I (0)
is equiphasic, the flow of current is toward lead aVF, be-
cause lead aVF is perpendicular to lead I. If the flow of
current is toward 90, which is the positive side of aVF,
the tallest deflection will be recorded in aVF (Fig. 4.5A).
If the flow of current is toward 90 away from the
Leads II and aVL Leads III and aVR
-120 - 60
0
0 aVR
- 30 0
- 150
aVL
I
0
0
0
0 +30
+150
II 0
III
0
+ 60 + 120
C
positive side of aVF, lead aVF will record the deepest
deflection (Fig. 4.5B).
Figures 4.5C and D summarize the possible deflections
of the other leads in the frontal plane if lead I is
equiphasic.
Lead II is equiphasic: If lead II (60) is equiphasic,
the flow of current is in the direction of lead aVL, be-
cause lead aVL is perpendicular to lead II. If the electri-
cal current is directed toward 30, the tallest deflec-
tion will be recorded in lead aVL (Fig. 4.6A) because
this is the positive side of lead aVL. On the other hand,
if the flow of current is toward 150, lead aVL will
record the deepest deflection, because this is away from
the positive side of lead aVL (Fig. 4.6B).
Figures 4.6C and D summarize the possible deflections
of the different leads in the frontal plane of the ECG if
lead II is equiphasic.
Lead III is equiphasic: If the QRS complex in lead III
(120) is equiphasic, the flow of current is in the direc-
tion of lead aVR, because lead aVR is perpendicular to
lead III. If the electrical current is directed toward
150, the tallest deflection will be recorded in lead aVR
(Fig. 4.7A) because this is the positive side of lead aVR.
On the other hand, if the flow of current is toward 30,
lead aVR will record the deepest deflection because this
is the negative side of lead aVR (Fig. 4.7B).
Figures 4.7C and D summarize the possible deflections
of the different leads in the frontal plane if lead III is
equiphasic.
Figuring Out the Axis of the QRS
Complex; Summary and Practice
Tracings
When an isoelectric deflection is recorded in any lead
in the frontal plane, the mean axis of the QRS complex
can be easily calculated (Figs. 4.84.13).
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The Electrical Axis and Cardiac Rotation 33

0 0
-90 0 -90 Figure 4.5:Lead I is
-120
Equiphasic. If the QRS
complex in lead I is equiphasic
(A, B), lead aVF will register the
180 - + 00 I 180 - + 00 tallest deflection if the current is
I
directed toward the positive side
of aVF at 90 (A) and the deep-
est deflection if the current is di-
0 0 rected toward 90, away from
+90 +90
aVF the positive side of aVF (B). The
aVF
electrocardiogram configuration
of the other leads if lead I is
A B
equiphasic is summarized in
C and D.
0 0
-90 -90
aVR
aVL aVR
0 aVL
0 0
-150 -30
0 -150 -30

180
0 - + 0 180
0 - +00
0 I I

0 0 0
+120 0 +60 0 0 +60
+90 +120 +90
III aVF II aVF II
III
C D

0 0
-90 0 -90 Figure 4.6: Lead II is
-120
aVL aVL Equiphasic. If the QRS
0 0
-30 -30 complex in lead II is equiphasic
(A, B), lead aVL will register the
180 - + 00 180 - + 00 tallest deflection if the current is
I I
moving toward 30, which is the
0 0
positive side of aVL (A). If the
+150 +150 electrical current is moving away
0 0
0 +60 0 +60 from the positive side of lead aVL
+90 +90
II II or toward 150, lead aVL will
aVF aVF
B record the most negative deflec-
A
tion (B). The configuration of the
electrocardiogram in the other
0 0
-90 -90 leads is summarized in C and D.
aVR aVL aVR aVL
0 0 0 0
-150 -30 -150 -30

180
0 - + 0 180
0 - +00
0 I I
0 0
+150 +150
0 0 0
+120 0 +60 +120
0
0 +60
+90 +90
III aVF II III aVF II

C D
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34 Chapter 4

0 0
Figure 4.7: Lead III is aVR -90 0 aVR -90 0
-60 -60
Equiphasic. If the QRS 0
complex in lead III is equiphasic -150
0 -150
(A, B), lead aVR will register the
tallest deflection if the current is 180
0 - + 00 0
180 - + 00
I I
moving toward 150, which is
the positive side of aVR (A). If the 0
+30
0 +30
current is moving away from the +
+
positive side of lead aVR toward +120
0 0 +120
0 0
+90 +90
30, lead aVR will record the III aVF III aVF
most negative deflection (B). The B
A
configuration of the electrocar-
diogram in the other leads when
lead III is equiphasic is 0
-90 0
0
-90
summarized in C and D. -60 aVR 0
aVR aVL -60
-150
0
0 0
aVL
-30 -150 -30
0

- + 0 0 - +00
180
0 0 I 180 I

0 0
+120 0 +60 0 +60
0
+90 +120 0
III aVF II +90 II
III aVF
C D

Figure 4.8: Isoelectric

Deflection in Lead I. Lead I is
isoelectric. Because lead I is
perpendicular to aVF, and lead I 00
aVF has a tall complex, the axis
is 90.

aVF
900

Figure 4.9: Isoelectric

Deflection in aVL. Lead aVL is
aVL
isoelectric. Because lead aVL is
-300
perpendicular to lead II, and lead
II shows the tallest deflection, the
axis is +60.

II
600
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The Electrical Axis and Cardiac Rotation 35

Figure 4.10: Isoelectric De-

-60 0 flection in aVR. Lead aVR is
-1500 isoelectric. Because aVR is
aVR perpendicular to lead III, and lead
III has the deepest complex, the
axis is 60. Note that tall R
waves are present in aVL (30),
which is beside the negative side
of lead III.
III
1200

-1500
aVR

300

III
1200

Figure 4.11: Isoelectric Deflection in III. Lead III is isoelectric. Because III is perpendicular to lead aVR,
and lead aVR has a negative complex, the axis is away from the positive side of aVR or 30. This is substan-
tiated by the presence of tall R waves in leads I and lead II. These leads flank the negative side of lead aVR.

I 00

aVF
900

Figure 4.12: Isoelectric Deflection in aVF. Lead aVF is isoelectric. Because aVF is perpendicular to
lead I, and lead I has the tallest complex, the axis is 0.
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36 Chapter 4
Figure 4.13:
Isoelectric Deflection
in aVR. Lead aVR is iso-
electric. Because aVR is
perpendicular to lead III,
and lead III has the tallest
complex, the axis is 120.
The diagrams in Figure 4.14 summarize how to rapidly
assess the axis of the QRS complex when an equiphasic
complex is present.
Method 2
As shown in the previous examples, the axis of the QRS
complex can be calculated rapidly using the eyeball
technique when an isoelectric complex is present in any
lead in the frontal plane. Not all ECGs, however, will have
an isoelectric complex. If an isoelectric complex is not
present, the mean QRS axis can be estimated just as rap-
idly by the following method.
Select the smallest QRS complex: The axis is ob-
tained using the same method as calculating the axis
when an isoelectric complex is present.
n Thus, in Figure 4.15, lead aVL is selected because
the complex is the smallest and is almost isoelec-
tric. Lead aVL is perpendicular to lead II.
Because lead II shows the tallest complex, the
axis is approximately 60. Adjustment has to be
made to correct for the actual axis because the
complex in lead aVL is not actually isoelectric.
n Because aVL is negative (R  S), the axis is ad-
justed further away from 60, thus the axis is ap-
proximately 70 rather than 60.
n Had aVL been positive (R  S), the axis is adjusted
closer to 50 rather than 70.
Method 3: Plotting the Amplitude of the QRS
Complex using Two Perpendicular Leads
If there are no isoelectric complexes in the frontal plane, a
simple way of calculating the axis is to select any pair of
leads that are perpendicular to each other like leads I and
aVF. The ECG in Figure 4.15 does not show any isoelectric
QRS complex and will be used for calculation. The QRS
complexes in leads I and aVF are shown in Figure 4.16.
Step 1: The total amplitude of the QRS complex in
lead I is 4 units. This is measured by subtracting
any upright deflection from any downward deflec-
tion (R 5 units, S 1 unit; total 4 units).
-600
-1500
aVR
III
1200
Step 2: The total amplitude of the QRS complex in
lead aVF is 9 units.
Step 3: Perpendicular lines are dropped for 4 units
from the positive side of lead I and for 9 units from
the positive side of lead aVF until these two lines in-
tersect (Fig. 4.16). The point of intersection is
marked by an arrowhead and connected to the cen-
ter of the hexaxial reference system. The line drawn
represents a vector, which has both direction and
magnitude. The direction of the vector is indicated
by the arrowhead. Thus, the mean electrical axis of
the QRS complex is 70.
The diagram in Fig. 4.17 summarizes the different
ECG deflections that will be recorded if several unipo-
lar recording electrodes are placed along the path of
an electrical impulse traveling from left to right to-
ward 0:
The electrode at 0 will record the most positive de-
flection.
The electrode at 180 will show the most negative
deflection.
The electrode perpendicular to the direction of the
impulse (90 and 90) will record an equiphasic
or isoelectric complex.
Any recording electrode that is located within 90 of
the direction of the electrical current (checkered
area) will record a positive deflection (R  S wave).
Any electrode that is further away and is 90 of the
direction of the electrical impulse will show a nega-
tive deflection (R  S wave).
The diagrams in Fig. 4.18 summarize the location of
the QRS axis when an equiphasic QRS complex is not
present in the frontal plane (Fig. 4.18).
The Precordial Leads
Horizontal plane: The six precordial leads V1 to V6 are
also called horizontal or transverse leads since they
represent the horizontal or transverse plane of the
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The Electrical Axis and Cardiac Rotation 37

-900 -900 -900

180 00 I 180 00 I 180 00 I

+900 +900 +900

0
aVF +90 aVF -90 0 aVF 00

-900 aVL aVL

-300 -300

180 00 I
+1500 +1500

+600 +600
II II
+900
0
aVF 1800 -30 +1500

-1200 aVL -1200 aVL

0
-30 -300 -600
aVR
-1500

+1500 +1500

+600 +600 +300

II II
+1200
0 0
+60 -120 III -1500

-600 -600 -600

aVR aVR aVR
-1500 -1500 -1500

+300 +300 +300

+1200 +1200 +1200

III +300 III +1200 III -600

Figure 4.14: Diagrams Showing the Location of the QRS. Bold arrows point to the QRS axis when an
equiphasic complex is present.
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38 Chapter 4

SUP
-1200 -900
-600
-1500 -300
aVR aVL

R +1800 I 00 L

+300

III II
+1200 aVF +600
+900
INF

Figure 4.15: Figuring Out the Axis when no Isoelectric Complex is Present. Lead aVL is selected
because the complex is the smallest and almost isoelectric. Lead aVL is perpendicular to lead II. Because lead II
shows the tallest complex, the axis is close to 60. Lead aVL, however, is not actually isoelectric but is negative (r 
S); thus, the axis of the QRS complex is adjusted further away and is closer to 70 (dotted arrow) than 60.

chest. The horizontal plane includes the left/right as

well as the anteroposterior sides of the chest (Fig. 4.19).
Leads V1 and V2: Leads V1 and V2 are right-sided
precordial leads and are positioned directly over the -900
right ventricle. The QRS complexes in V1 and V2
represent electrical forces generated from the right

1800 00

+4 +900
I 00
Lead I = 4 units Lead aVF= 9 units

+9
aVF + 700
+ 900
Figure 4.16: Figuring the QRS Axis. The electrocardiogram
showing leads I and aVF. The total amplitude of the QRS complex
of 4 units is identified on the positive side of lead I. The total
amplitude of 9 units is also identified on the positive side of
lead aVF. Lines are dropped perpendicularly from leads I and
aVF until the line intersects. The lines intersect at 70, which
mark the axis of the QRS complex.
Figure 4.17: The Electrocardiogram Configurations of
an Electrical Impulse Traveling Toward 0. The diagram
summarizes the different electrocardiogram configurations of
an impulse traveling at 0 if several electrodes are placed along
its path. Any lead within 90 of the direction of the electrical im-
pulse (checkered area) will record a positive deflection. Any lead
that is further away (90) will record a negative deflection. The
most positive or tallest deflection is recorded by the electrode
positioned at 0 and the most negative by the electrode at 180.
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The Electrical Axis and Cardiac Rotation 39

(I = Rs, aVF = Rs) (I = rS, aVF = Rs) (I = Rs, aVF = rS)

-900 -900 -900

+180 - 00 I +180 - 00 I +180 - 00 I

+900 Normal +900 Right +900 Left

aVF Axis aVF Axis aVF Axis

(I = rS, aVF = rS) (II = Rs, aVL = Rs) (II = Rs, aVL = rS)
-900 0
-120 aVL -1200 aVL
-300 -300

+180 - 00 I

+1500 +1500

+600 +600
+90 0
NW II II
0 0 0 0
aVF Axis -30 to+60 +60 to +150

(II = rS, aVL = rS) (II = rS, aVL = Rs)

-1200 aVL -1200 aVL
-300 -300

+1500 +1500

+600 +600
II II
0 0 0 0
+150 to -120 -30 to -120

Figure 4.18: Checkered Area shows the Location of the QRS Axis when an Equiphasic QRS Com-
plex is Not Present. NW, northwest.

ventricle and generally show small r and deep S
waves.
Leads V5 and V6: Leads V5 and V6 are left-sided pre-
cordial leads that directly overlie the left ventricle.
The QRS complexes represent electrical forces gen-
erated from the left ventricle, which show small q
waves followed by tall R waves.
Leads V3 and V4: The QRS complexes are equipha-
sic in leads V3 and V4 because these leads represent
the septal area and is the transition zone between
the deep S waves in V1 and V2 and the tall R waves in
V5 and V6 (Fig. 4.19).
Cardiac Rotation
Cardiac rotation: In the horizontal plane, a change in
the electrical position of the heart is described as rota-
tion. The heart may rotate clockwise or counterclock-
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40 Chapter 4

Posterior Counterclockwise rotation or early transition:

Right LV 0 Left
V6 0
RV
V5 0
30
V1 V4
V2 V3 60 0
1200 900 75
0
Anterior
Figure 4.19: Precordial Leads V1 to V6. The location of
the precordial leads and the expected normal configuration of
the QRS complexes from V1 to V6 are shown. The QRS complex is
equiphasic in V3, which is circled. V3 and V4 represent the transi-
tion zone between the deep S waves in V1 and V2 and the tall R
waves in V5 and V8. LV, left ventricle; RV, right ventricle.
wise (Fig. 4.20), resulting in a shift of the transition
zone to the left or to the right of V3 or V4.
Clockwise rotation or delayed transition: When
the heart rotates clockwise, the transition zone,
which is usually in V3 or V4, moves to the left toward
V5 or V6. This is called clockwise rotation, delayed
Tall R Waves in V1
transition, or late transition. When the apex of the
heart is viewed from under the diaphragm, the front
of the heart moves to the left, causing the right ven-
tricle to move more anteriorly (Fig. 4.20A).
When the heart rotates counterclockwise, the transi-
tion zone moves earlier, toward V1 or V2. This is
called counterclockwise rotation or early transition.
When the apex of the heart is viewed from under the
diaphragm, the front of the heart moves to the right
causing the left ventricle to move more anteriorly
(Fig. 4.20C).
In cardiac rotation, it is important to recognize that the
heart is being visualized from under the diaphragm
looking up. This is opposite from the way the precor-
dial electrodes are conventionally visualized, which is
from the top looking down. Thus, in cardiac rotation,
the anterior and posterior orientation of the body and
the direction of cardiac rotation is reversed (compare
Fig. 4.19 and 4.20).
Rotation of the heart is determined by identifying the
transition zone where the QRS complex is equiphasic
(Fig. 4.21). Rotation is normal if the transition zone is
located in V3 or V4 (Fig. 21A, B). Figures 4.21C and D
show counterclockwise rotation or early transition,
and Figures 4.21E and F show late transition or clock-
wise rotation. The transition zones are circled (Figs.
4.224.24).
R wave taller than S wave in V1: In children, the R
wave may be taller than the S wave in V1. This is un-
usual in adults (Figs. 4.25A and 4.26, normal ECG).

A: Clockwise Rotation B: Normal Rotation C: Counterclockwise

Rotation

A A A
V1 V1 V1 CCW
CW
RV
RV
V6 V6
R V6 R LV
L R RV LV
LV L
L

P P P

Figure 4.20: Clockwise and Counterclockwise Rotation. Rotation of the heart is viewed from under the
diaphragm. (A) Clockwise rotation. The front of the heart moves to the left as shown by the arrow causing the right
ventricle to move more anteriorly. (B) Normal rotation. (C) Counterclockwise rotation. The front of the heart moves
to the right causing the left ventricle to move more anteriorly. A, anterior; CCW, counterclockwise rotation; CW,
clockwise rotation; L, left; LV, left ventricle; P, posterior; R, right; RV, right ventricle.
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The Electrical Axis and Cardiac Rotation 41

A
Figure 4.21: Transition Zones. (A, B) Nor-
R L mal transition where the R and S waves are
A equiphasic in V3 or V4. (C, D) Early transition or
P
counterclockwise rotation with the transition
zone in V1 or V2. (E, F) Late transition or
A
clockwise rotation with the equiphasic QRS
R L complex in V5 or V6. The transition zones are cir-
B
cled. A, anterior; P, posterior; R, right; L, left.

R L
C
P

R L
D
P

R L
E
P

R L
F
P

Figure 4.22: Normal Rotation.

Precordial leads V1 to V6 are shown.
There is gradual progression of the R
waves from V1 to V6. V4 is equiphasic
(circled), representing the normal
transition zone.

V2
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42 Chapter 4

Figure 4.23: Counterclockwise

Rotation or Early Transition.
There is early transition of the QRS
complexes with the equiphasic zone in
V1. This represents counterclockwise
rotation or early transition.

When R wave is taller than the S wave in V1, the follow-
ing should be excluded before this finding is considered
a normal variant.
Right bundle branch block (RBBB)
Right ventricular hypertrophy
Pre-excitation or Wolff Parkinson White (WPW)
ECG
Straight posterior myocardial infarction (MI)
Pacemaker rhythm
Ventricular ectopic impulses
RBBB: In RBBB, the QRS complexes are wide measur-
ing 0.12 seconds (Figs. 4.25B and 4.27). This is the
most important feature distinguishing RBBB from the
other entities with tall R waves in V1. Terminal R
waves are also present in V1 and wide S waves are pres-
ent in V5 and V6 or lead I (see Chapter 10, Intraven-
tricular Conduction Defect: Bundle Branch Block).

Figure 4.24: Clockwise Rotation

or Late Transition. There is gradual
progression of the R wave from V1 to V6
until the QRS complex becomes
equiphasic in V6. This represents clock-
wise rotation or late transition.
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The Electrical Axis and Cardiac Rotation 43

A B C D E F G

Figure 4.25: Tall R Wave in V1. (A) Normal electrocardiogram. The R wave is smaller than the S wave.
(B) Right bundle branch block. (C) Right ventricular hypertrophy. (D) Pre-excitation. (E) Straight posterior myocardial
infarction. (F) Pacemaker-induced ventricular complex. (G) Ectopic ventricular complexes from the left ventricle.

Figure 4.26: Normal Electrocardiogram. Note that the R waves are smaller than the S waves in V1.

Figure 4.27: Right Bundle Branch Block. The QRS complexes are wide and tall terminal R waves are present
in V1.
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44 Chapter 4

Figure 4.28: Right Ventricular Hypertrophy. When right ventricular hypertrophy is the cause of the tall R
waves in V1, right axis deviation of 90 is almost always present. The diagnosis of right ventricular hypertrophy is
unlikely if the axis is not shifted to the right.

Right ventricular hypertrophy: In right ventricular
hypertrophy, a tall R wave in V1 is almost always associ-
ated with right axis deviation of approximately 90
(Figs. 4.25C and 4.28). The diagnosis of RVH is uncer-
tain unless there is right axis deviation in the frontal
leads.
Pre-excitation or WPW ECG: In WPW syndrome, ev-
idence of pre-excitation is present in the baseline ECG
with short P-R interval and presence of a delta wave.
The R waves are tall in V1 when the bypass tract is left-
sided (Figs. 4.25D and 4.29).
Posterior MI: Straight posterior MI is usually seen in
older patients, not in children or young adults. It is of-
ten associated with inferior MI with pathologic q waves
in leads II, III, and aVF (Figs. 4.25E and 4.30) or history
of previous MI.
Pacemaker rhythm: When the rhythm is induced
by an artificial pacemaker, a pacemaker artifact al-
ways precedes the QRS complex. Generally, a pace-
maker-induced QRS complex has a QS or rS config-
uration in V1 because the right ventricle is usually
the chamber paced. However, when the R wave is tall
in V1 and is more prominent than the S wave (R or
Rs complex), left ventricular or biventricular pacing
should be considered as shown in Figures 4.25F
and 4.31 (see Chapter 26, The ECG of Cardiac Pace-
makers).
Ventricular ectopic impulses: Ventricular ectopic
impulses may show tall R waves in V1. This can occur
when the ectopic impulses originate from the left ven-
tricle (Figs. 4.25G and 4.32).
Normal variant: The ECG is shown (Fig. 4.33).

Figure 4.29: Pre-excitation (Wolff Parkinson White Electrocardiogram). A short P-R interval with delta
wave (arrows) from pre-excitation is noted. In pre-excitation, the R waves are tall in V1 when the bypass tract is left-sided.
LWBK271-C04_30-47.qxd 1/30/09 11:23 AM Page 45 Aptara Inc.

Figure 4.30: Posterior Myocardial Infarction. In posterior myocardial infarction (MI), tall R waves in V1 is
usually associated with inferior MI. Note the presence of pathologic q waves in leads II, III, and aVF.

Figure 4.31: Pacemaker-induced QRS Complexes. Tall R waves in V1 from pacemaker-induced rhythm. Ar-
rows point to the pacemaker artifacts.

Figure 4.32: Wide Complex Tachycardia with Tall R Waves in V1. Tall R waves in V1 may be due to ectopic
impulses originating from the left ventricle.

45
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46 Chapter 4

Figure 4.33: Normal Variant. The electrocardiogram shows tall R waves in V1 and V2 in a patient with
completely normal cardiac findings. Before considering tall R waves in V1 and V2 as normal variant, other causes
should be excluded.

in V1. This often occurs when there is mitral steno-

Clockwise Rotation
Clockwise rotation: In clockwise rotation or late transi-
tion, the transition zone of the QRS complexes in the
precordial leads is shifted to the left of V4 resulting in
deep S waves from V1 to V5 or often up to V6 (Fig. 4.34).
Clockwise rotation is usually the result of the following:
Left ventricular hypertrophy: This can be due to
several causes, including dilated cardiomyopathy or
left-sided valvular insufficiency.
Right ventricular hypertrophy: Depending on
the cause of the right ventricular hypertrophy,
clockwise rotation may be present instead of a tall R
sis, pulmonary hypertension and chronic obstruc-
tive pulmonary disease (see Chapter 7, Chamber
Enlargement and Hypertrophy).
Biventricular hypertrophy: Both ventricles are
enlarged.
Chronic obstructive pulmonary disease: In
chronic obstructive pulmonary disease such as em-
physema or chronic bronchitis, the diaphragm is
displaced downward causing the heart to rotate
clockwise and become vertically oriented (Fig.
4.34).
Acute pulmonary embolism: See Chapter 7,
Chamber Enlargement and Hypertrophy.

Figure 4.34: Clockwise Rotation. In clockwise rotation, the transition zone is shifted to the left, resulting in
deep S waves from V1 to V6. Note that the R waves are smaller than the S wave in V5 and in V6 because of a shift in
the transition zone to the left of V6. The electrocardiogram also shows right axis deviation; peaked P waves in II, III,
and aVF; and low voltage in lead I. The cardiac rotation is due to chronic obstructive pulmonary disease.
LWBK271-C04_30-47.qxd 1/30/09 11:23 AM Page 47 Aptara Inc.
Left anterior fascicular block: See Chapter 9, In-
traventricular Conduction Defect: Fascicular Block.
Other causes: Cardiac rotation resulting from shift
in mediastinum or thoracic deformities including
pectus excavatum.
Suggested Readings
Burch GE, Winsor T. Principles of electrocardiography. In: A
Primer of Electrocardiography, 5th ed. Philadelphia: Lea and
Febiger; 1966:1766.
The Electrical Axis and Cardiac Rotation 47
Burch GE, Winsor T. Precordial leads. In: A Primer of Electrocar-
diography, 5th ed. Philadelphia: Lea and Febiger; 1966:
146184.
Dunn MI, Lippman BS. Basic ECG principles. In: Lippman-
Massie Clinical Electrocardiography, 8th ed. Chicago: Year-
book Medical Publishers; 1989:5162.
Marriott HJL. Electrical axis. In: Practical Electrocardiography,
5th ed. Baltimore: Willliams & Wilkins; 1972:3443.
Wagner GS. Cardiac electrical activity. In: Marriotts Practical
Electrocardiography, 10th ed. Philadelphia: Lippincott
Williams & Wilkins; 2001;219.
Wagner GS. Recording the electrocardiogram. In: Marriotts
Practical Electrocardiography, 10th ed. Philadelphia: Lippin-
cott Williams & Wilkins; 2001;2641.
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5
Heart Rate and Voltage

Height: The height represents voltage. Because the

The ECG Paper
The standard electrocardiogram (ECG) is recorded at a
paper speed of 25 mm per second. The voltage is cali-
brated so that 1 mV gives a vertical deflection of 10 mm.
ECG paper: The ECG paper consists of parallel vertical
and horizontal lines forming small squares 1 mm wide
and 1 mm high. Every fifth line is highlighted and is
darker than the other lines, thus defining a larger
square of five small squares vertically and horizontally.
An example of an ECG is shown in Figure 5.1.
Width: The width of the ECG paper represents time.
Every millimeter or one small block is equivalent to
0.04 seconds, because the ECG records with a paper
speed of 25 mm/second. Every highlighted line con-
taining five small squares is equivalent to 0.20 seconds.
height is standardized to give a deflection of 10 mm
per mV, every small square is equivalent to 0.10 mV.
The calibration marker is routinely recorded at the
beginning or end of a 12-lead tracing (Fig. 5.1).
Calculating the Heart Rate
There are several methods of calculating the heart rate
from the ECG.
Using the large boxes: The heart rate, expressed
in beats per minute (bpm), can be calculated by
counting the number of large boxes between two R
waves (Fig. 5.2).
Using the small boxes: Another method of calculat-
ing the heart rate is by counting the number of small

1 mm = 0.10 mV
1 mm = 0.04 second
1 mm = 0.04 second
1 mm = 0.10 mV
0.50 mV

0.20 second

0.50 mV
Calibration marker
0.20 second

1.0 mV = 10 mm

Figure 5.1: The Electrocardiogram (ECG) Paper. The ECG paper is divided into small squares. The width
of the smallest square is 1 mm, which is equivalent to 0.04 seconds. The height of the smallest square is 1 mm,
which is equivalent to 0.10 mV. When a 12-lead ECG is obtained, a calibration signal is routinely recorded such
that 1.0 mV gives a deflection of 10 mm.

48
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1 2 3 4 5 6 7 8
300 1 =
300 Heart rate per minute
300 2 = 150
300 3 = 100
300 4 = 75
300 5 = 60
300 6 = 50
300 7 = 43
300 8 = 38
300 9 = 33
Heart rate per minute = 300 Number of large squares
boxes between two R waves. This is the most accurate
method when the heart rate is regular and fast (Fig. 5.3).
Using 3-second time markers: A third method of
calculating the heart rate is by using the 3-second
time markers, which are printed at the top margin of
the ECG paper. The distance between the time
markers is 3 seconds. The heart rate is calculated by
counting the number of QRS complexes within 3
seconds and multiplied by 20. The first complex is
the reference point and is not counted (Fig. 5.4).
Using 6-second time markers: If the heart rate is
irregular or very slow (Fig. 5.5), a longer time inter-
val such as 6-second time marker or even 12-second
time marker is chosen. The heart rate is calculated
by counting the number of QRS complexes within 6
seconds and multiplied by 10. If 12 seconds are
used, the number of complexes is multiplied by 5, to
obtain the heart rate per minute.
Not all ECG papers have 3-second time lines. A 3-
second time line, however, can be created by count-
ing 15 large blocks in the ECG paper. Similarly, a
Heart Rate and Voltage 49
Figure 5.2: Calculating the
Heart Rate Using the Large
Squares. The heart rate can be
calculated by the formula 300 
the number of large squares
9 Number between two R waves. Thus, if there
of large are 5 large squares between 2 QRS
squares complexes, the heart rate is 60
beats per minute (300  5  60).
6-second time line can be created by counting 30
large blocks.
Using commercially available heart rate sticks:
Several commercially available heart rate meters can
be used to calculate heart rates. The meter is placed
on the ECG rhythm strip and the heart rate is read
directly from the meter stick as shown (Figs. 5.6 and
5.7). Using a heart rate meter stick is a very conven-
ient way of measuring heart rates. Unfortunately,
they are not always available when needed.
Using a heart rate table: When the heart rate is reg-
ular, a heart rate table can be used for calculating
heart rates. When calculating heart rates, it is more
convenient to use the larger boxes for slower heart
rates and the smaller boxes for fast heart rates if the
heart rate is regular. Note that the same heart rate can
be obtained by using the formula 300 divided by the
number of big boxes or 1,500 divided by the number
of small boxes, as explained earlier. If the heart rate is
irregular as in patients with atrial fibrillation, a 6- or
12-second rhythm strip is more accurate (Fig. 5.8).
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50 Chapter 5

Figure 5.3: Calculating the

Heart Rate Using the Small
Squares. Using the small squares,
the heart rate can be calculated by the
formula 1,500  the number of small
boxes between two R waves. Thus, if 5 7 9 11 13 15 17 19 21 Number of small squares
there are 5 small squares between 2 1500 5 =
QRS complexes, the heart rate is 300 300 Heart rate per minute
beats per minute (1,500  5  300).
1500 7 =
188

1500 9 = 167

1500 11 = 136

1500 13 = 116

1500 15 = 100

1500 17 = 88

1500 19 = 79

1500 21 = 71

Heart rate per minute = 1500 Number of small squares

HR = 7 X 20 = 140 BPM
3 seconds
0 1 2 3 4 5 6 7

Figure 5.4: Calculating the Heart Rate Using the 3-Second Time Markers. There
are seven complexes within the 3-second time line.The heart rate is 7  20  140 beats per
minute. Note that the first QRS complex is the reference point and is not counted.

HR = 4 X 10 = 40 BPM
6 seconds

0 1 2 3 4

Figure 5.5: Calculating the Heart Rate Using the Time Markers. Because the heart
rate is very slow, a longer interval is measured and two 3-second markers (6 seconds) are
used. There are four complexes within the 6-second time line. Thus, the heart rate is 4  10 
40 beats per minute.
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0 1 2 Figure 5.6: Heart Rate Meter Stick

Using Two Cardiac Cycles. An example
of a heart rate meter stick is shown. This
heart rate stick uses two cardiac cycles to
Heart measure the heart rate. Two QRS complexes
Rate
are measured starting from the reference
Stick
point, which is identified by an arrow on the
left side of the meter stick. The heart rate is
Heart Rate = 76 BPM read directly from the meter stick and is 76
Start Here
beats per minute.

Start Here Heart Rate = 76 BPM Figure 5.7: Heart Rate Meter Stick
Using Three Cardiac Cycles. This particu-
lar meter stick uses three cardiac cycles to cal-
culate the heart rate. Three cardiac cycles are
counted starting from the reference point,
which is at the left side of the meter stick. The
heart rate is read directly from the meter stick
and is 76 beats per minute.
0 1 2 3

300
= Heart Rate per Minute
Number of Large Boxes
Reference
Point
Number of Large Boxes

HR = 300 150 100 75 60 50 43 38 33

1 2 3 4 5 6 7 8 9

5 10 15 20 25 30 35 40 45

HR = 300 150 100 75 60 50 43 38 33

250 136 94 71 58 48 42 37
214 125 88 68 56 47 41 36
188 115 83 66 54 45 39 35
167 107 79 63 52 44 38 34

Reference Number of Small Boxes

Point
1500
= Heart Rate per Minute
Number of Small Boxes

Figure 5.8: Figuring the Heart Rate. When the rhythm is regular, the heart rate can be calculated by measuring
the distance between two QRS complexes using the large boxes (upper portion of the diagram) or the small boxes
(lower portion of the diagram). The larger boxes are more convenient to use when the heart rate is 100 beats per
minute, whereas the smaller boxes are more accurate to use when the heart rate is faster and 100 beats per minute.
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52 Chapter 5

Figure 5.9: Tall Voltage. Two sets A: Normal Standard B: Half Standard
of electrocardiograms (ECGs) were ob- Calibration signal
tained from the same patient 10 mm = 1.0 mV Calibration signal
5 mm = 1.0 mV
representing the precordial leads and a
lead II rhythm strip. (A) The ECG was
recorded at normal calibration. Note
that the amplitude of the QRS
complexes is very tall with the calibra-
tion set at normal standard voltage
(10 mm  1.0 mV). (B) The ECG was
recorded at half standard voltage (5
mm  1.0 mV). Note that the
amplitude of the QRS complexes is
smaller, the ECG is less cluttered, and
the height of the QRS complexes is eas-
ier to measure. The calibration signals
are recorded at the end of each tracing II II
and are marked by the arrows.

Low voltage: Excess fat, fluid, or air does not conduct

ECG Voltage
Voltage: The height or amplitude in the ECG paper
represents voltage. The calibration signal is routinely
printed at the beginning or end of the 12-lead record-
ing (Fig. 5.9) and is standardized so that 1 mV gives a
deflection of 10 mm. If the QRS complexes are too
small (low voltage) or too tall (tall voltage), the stan-
dardization can be doubled or halved accordingly by
flipping a switch in the ECG machine.
Tall voltage: The voltage of the QRS complex is in-
creased when there is hypertrophy of the left ventricle.
This is further discussed in Chapter 7, Chamber En-
largement and Hypertrophy. The voltage in the precor-
dial leads is also normally taller in young individuals,
especially African American males, in patients who are
thin or emaciated, and in patients with mastectomy, es-
pecially of the left breast.
impulses well and will attenuate the size of the com-
plexes. The distance between the heart and the record-
ing electrode will also influence the voltage in the ECG.
Thus, the complexes in the limb leads are smaller than
the complexes in the precordial leads because the loca-
tion of the limb electrodes is farther from the heart.
Fluid around the heart, lungs, abdomen, body, or ex-
tremities as well as obesity will also attenuate the size of
the complexes. The low voltage may be generalized or it
may be confined to the limb or frontal leads.
Low voltage in the limb leads: Low voltage confined
to the limb leads indicates that not a single QRS com-
plex measures 5 mm (0.5 mV) in any of the frontal or
limb leads. The voltage in the chest leads is normal.
Generalized low voltage: Generalized low voltage
indicates that not a single QRS complex measures 5
mm (0.5 mV) in the limb leads and 10 mm (1.0 mV)
in the chest leads (Fig. 5.10).

Calibration signal
Figure 5.10: Low Voltage with 10 mm = 1.0 mV
Electrical Alternans. Twelve-lead
electrocardiogram showing general-
ize low voltage. Note that not a single
QRS complex measures 5 mm in the
limb leads or 10 mm in the precordial
leads. In addition, there is also beat-
to-beat variation in the size of the
QRS complexes because of electrical
alternans (arrows). The presence of a
large pericardial effusion was verified
by an echocardiogram.
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Electrical Alternans
In electrical alternans, there is a beat-to-beat variation in the
size of the QRS complexes usually by 1 mm. An example
of alternating voltage of the QRS complex resulting from
significant pericardial effusion is shown in Figure 5.10.
Calculating the Heart Rate and
Measuring the Voltage
ECG Findings
Heart rate: The number of heartbeats per minute can be
counted accurately using the ECG.
Voltage: The voltage of any wave in the ECG can also be
measured by its amplitude.
Mechanism
Heart rate: The QRS complex represents activation of the
ventricles, which causes the heart to pump blood to the dif-
ferent parts of the body. The heart beat per minute can be
counted by palpating the radial pulse or more accurately by
counting the number of QRS complexes in the ECG.
Voltage: The height of the different complexes in the ECG
depends on a number of factors, which can either increase or
decrease their amplitude. Increased ventricular mass and
close proximity of the recording electrode to the origin of the
impulse will enhance the voltage. On the other hand, the pres-
ence of fat, fluid, or air and a longer distance between the ori-
gin of the impulse and the recording electrode will attenuate
the voltage in the ECG.
Clinical Implications
Heart rate: Included as one of the vital signs in the evalua-
tion of any patient is the heart rate. When the patient is on a
cardiac monitor, the heart rate is displayed together with the
ECG rhythm. The heat rate can also be obtained very accu-
rately in a recorded ECG. This can be done rapidly by meas-
uring the distance between two R waves when the heart rate
is regular. If the heart rate is irregular, a longer rhythm strip
is needed for a more precise reading. Note that the heart rate
obtained by ECG is more accurate than the pulse rate ob-
tained at bedside because not all the impulses recorded in the
ECG may be strong enough to generate a cardiac output that
is palpable as a pulse, especially in sick patients who are hy-
potensive or in heart failure or when the patient has an irreg-
ular rhythm. In these patients, the pulse rate is not always
equal to the heart rate.
Regular heart rate: When the rate is 100 bpm, the
larger boxes are more convenient to use. When the rate is
100 bpm, the smaller boxes are more convenient and
more accurate to use. The distance between two QRS
complexes in large or small boxes is used for counting the
Heart Rate and Voltage 53
ventricular rate and the distance between two P waves for
counting the atrial rate.
n Large boxes: The heart rate per minute can be calcu-
lated using the formula: 300  number of large boxes
between two R waves. The formula is based on the fol-
lowing information.
n Standard ECG paper speed  25 mm per second or
1,500 mm per minute. Because one large box  5 mm,
ECG paper speed is 1,500  5, or 300 large boxes per
minute.
n Heart rate per minute  300  number of large boxes
between two QRS complexes.
n Small boxes: The heart rate per minute is obtained by
dividing 1,500 by the number of small boxes between
two R waves. The formula is derived from the follow-
ing information:
n Standard ECG paper speed  25 mm per second or
1,500 mm per minute.
n Heart rate per minute  1,500  number of small
boxes between two QRS complexes.
Irregular heart rate: When the heart rate is irregular
(atrial flutter or atrial fibrillation), a longer interval
should be measured to provide a more precise rate. A 3-
second time line can be created if it is not marked in the
rhythm strip. A 3-second interval is equal to 15 large
boxes.
n If a 3-second time interval is used, multiply the num-
ber of QRS complexes by 20.
n If a 6-second time interval is used, multiply the num-
ber of complexes by 10.
n If a 12-second time interval is used, multiply the num-
ber of complexes by 5.
n Note that the first QRS complex is used as a reference
point and is not counted.
Voltage: Tall voltage in the ECG suggests that there is in-
creased mass of the right or left ventricle. This is further dis-
cussed in Chapter 7, Chamber Enlargement and Hypertro-
phy. Decreased voltage of the QRS complex occur when
transmission of the cardiac impulse to the recording elec-
trode is diminished and are frequently seen in patients who
are obese or patients with chronic pulmonary disease, pleu-
ral or pericardial effusions, generalized edema, hypothy-
roidism, or when there is infiltrative cardiomyopathy, such as
in amyloidosis, causing reduction in the number of myocytes
in the ventricles and atria.
Electrical alternans: Alternating voltage of the QRS
complex can occur when there is significant pericardial
effusion, which allows the heart to swing in a pendular
fashion within the pericardial cavity. When the heart
moves closer to the chest wall, the QRS complex becomes
taller. When it is pushed further away from the chest wall
by the next beat, the QRS complex becomes smaller. The
alternating size of the QRS complex is best recorded in
the precordial electrodes especially V2 to V5 because these
leads are closest to the heart. Electrical alternans because
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54 Chapter 5

of pericardial effusion can occur only if the pericardial ef-
fusion is large enough to allow the heart to swing within
the pericardial cavity. Alternation of the QRS complex be-
cause of pericardial effusion is a sign of cardiac tampon-
ade. Electrical alternans can also occur even in the ab-
sence of pericardial effusion when there is abnormal
conduction of the electrical impulse in the ventricles al-
ternating with normal conduction. It can also occur dur-
ing supraventricular tachycardia or when there is severe
myocardial ischemia. Electrical alternans can involve any
wave of the ECG including P waves, QRS complexes, and
T waves.
Suggested Readings
Marriot HJL. Rhythm and rate. In: Practical Electrocardiography.
5th ed. Baltimore: Williams & Wilkins; 1972;1115.
Surawicz B, Fisch C. Cardiac alternans: diverse mechanisms and
clinical manifestations. J Am Coll Cardiol. 1992;20:483499.
LWBK271-C06_55-61.qxd 29/1/09 10:09 pm Page 55 LWBK270-4119G-C02_073-110.qxd
Depolarization and
Repolarization
Single Muscle Cell
Deflections in the electrocardiogram (ECG) includ-
ing the P waves, QRS complexes, and T waves are due
to depolarization and repolarization of the atria and
ventricles. The following discussion will provide a ba-
sic understanding of how these ECG deflections are
generated.
Every heartbeat is preceded by an electrical impulse
that originates from the sinus node. This impulse is
propagated from one cell to the next adjacent cell until
the whole myocardium is depolarized. After it is dis-
charged, the muscle cell immediately undergoes a
process of repolarization that permits the cell to again
depolarize at the arrival of the next impulse.
Single muscle cell: The resting potential of a single
muscle cell is approximately 90 mV with the inside of
the cell more negative than the outside (Fig. 6.1A). This
difference in potential makes the cell capable of being
discharged. When the myocardial cell is depolarized,
the polarity reverses with the inside of the cell becom-
ing more positive than the outside (Fig. 6.1B).
Depolarization of a Single Muscle Cell
Depolarization: During depolarization, the activa-
tion wave travels from one end of the myocardial cell to
the other end (Fig. 6.2A).
_ _ _ Muscle Cell at Rest and
+_ +_ +
_ +
_ Inside is + + +
+ + + _ _ _
+ __
negative _ +
_ _ _ _ _ _
Outside is _ +
+ _ +
_ ative to the outside. (B) During depolariza-
+ + + + positive
+ + +
A. Resting Myocardial Cell B. During Depolarization
6
Positive deflection: If a recording electrode is
placed in front of the traveling impulse (at position
1, Fig. 6.2B), a positive deflection is recorded.
Negative deflection: If a recording electrode is
placed behind the moving impulse (at position 2), a
negative deflection is recorded.
Moving dipole: A positive deflection is recorded
when the activation wave is advancing toward the
recording electrode because the activation wave is trav-
eling with the positive charge in front, which is facing
the recording electrode. When the activation wave is
moving away from a recording electrode, a negative de-
flection is recorded because the activation wave has a
negative charge behind, which is facing the recording
electrode. The activation wave in essence is a moving
vector with opposite charges, one positive and the
other negative. This moving vector with opposite
charges is called a dipole (Fig. 6.2B). During depolar-
ization, the dipole always travels with the positive
charge in front and the negative charge behind.
Repolarization of a Single Muscle Cell
Repolarization: Repolarization restores the polarity
of the cell to its original potential of 90 mV and is
recorded as a T wave in the ECG. In a single myocardial
cell, repolarization starts in the same area where the cell
was first depolarized, because this part of the cell has
had the most time to recover. The repolarization wave
Outside
Figure 6.1:
becomes
negative During Depolarization. (A) The resting
myocardial cell is negative inside the cell rel-
tion, the activation wave travels from one
Inside
becomes end to the other end, changing the polarity
positive inside the cell from negative to positive. Ar-
rows point to the direction of depolarization.
55
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56 Chapter 6

Zone of advancing
Figure 6.2: Depolarization. (A) The arrows
positive charges
indicate the direction of the activation wave, which _ _ _ _ _ +
_ +
_ +
_
is a zone of advancing positive charges.The front of + + + + +
the activation wave is circled. (B) The wave of depo- A
+_ +_ + + + _ _ _
larization is represented as a moving dipole with _ _ _
the positive charge traveling in front and the nega- + + +
tive charge behind. A recording electrode at posi-
tion 1 will record a positive deflection because the
+
_ +
_ +
_
dipole is traveling with the positive charge facing #1
#2
the electrode. A recording electrode at position 2 -+ _
will record a negative deflection since the electrode
_ _
is facing the negative charge of the moving dipole. + + +
Dipole
B

moves in the same direction as the wave of depolariza-

tion, only this time, the repolarization wave is a zone of
advancing negative charges (Fig. 6.3A). Thus, the di-
pole is traveling with the negative charge in front and
the positive charge behind (Fig. 6.3B).
Inverted T wave: During repolarization, the
recording electrode positioned in front of the repo-
larization wave (position 1, Fig. 6.3B) will record an
inverted T wave. This is because the electrode is fac-
ing the negative charge of the advancing dipole.
Upright T wave: The recording electrode placed
behind the repolarization wave (position 2) will
record an upright T wave because the electrode is
facing the positive charge of the moving dipole.
Depolarization and repolarization of a muscle
cell: Depolarization and repolarization of a single
muscle cell travel in the same direction. Thus, the R
wave and the T wave are inscribed in opposite direc-
tions.
Depolarization and Repolarization
of the Atria
Atrial depolarization and repolarization: The
atrial impulse originates from the sinus node and
spreads within the thin atrial wall in a circumferential
fashion until both atria are depolarized. Atrial depolar-
ization and repolarization parallels that of a single
muscle cell (Fig. 6.4).
DepolarizationP wave: Depolarization of the
atria occurs longitudinally with the impulse spread-
ing from one cell to the next adjacent cell. It is
recorded as a P wave in the ECG. Any electrode in
front of the advancing wave will record a positive
deflection. Any electrode behind the advancing
wave will record a negative deflection.
RepolarizationTa wave: Repolarization of the
atria is also represented by a T wave, but is more

Repolarization wave is
+ + + + + _ _ _ a zone of advancing
_ _ _ _ _ negative charges
+ + +
_ _ _ _ _ + + +
_ _ _
A + + + + +
_ _ _
+ + +
+-
#2 +_ +
_ +_ #1

B Dipole

Figure 6.3: Repolarization of a Single Muscle Cell. (A) The front of the repolar-
ization wave is circled and is a zone of advancing negative charges.The direction of the
repolarization wave is shown by the arrows. (B) A recording electrode in front of the
repolarization wave at position 1 will record an inverted T wave because the electrode is
facing the negative charge of the moving dipole. A recording electrode behind the repo-
larization wave at position 2 will record a positive or upright T wave because the
electrode is facing the positive charge of the moving dipole.
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Depolarization and Repolarization 57

Sinus Node
-+ +-
Atrial
Wall
-+ +-
A B
Depolarization Repolarization
(P wave)
-+ P +- (Ta wave)
Ta

Figure 6.4: Atrial Depolarization and Repolarization. (A) Depolarization

of the atria is represented as a P wave in the electrocardiogram.The impulse follows
the length of the thin atrial muscle and spreads circumferentially. (B) Repolarization
is represented as a Ta wave and follows the same direction as depolarization. Thus,
the P wave and the Ta wave are inscribed in opposite directions. Arrows represent
the direction of the spread of the electrical impulse.

specifically called a Ta wave to differentiate it from
the T wave of ventricular repolarization. Repolariza-
tion is similar to a single muscle cell and starts from
the area that was first depolarized because these cells
have had the longest time to recover. Any electrode
in front of the repolarization wave will record a neg-
ative deflection. The Ta wave is usually not visible
because the wave is too small to be recorded. When
present, it usually coincides with the QRS complex
in the ECG and is therefore obscured.
Depolarization and repolarization of the atria:
Similar to a single muscle cell, depolarization and repo-
larization of the atria follow the same direction. Thus, the
P wave and Ta wave are inscribed in opposite directions.
immediately adjacent to the epicardium, an upright
deflection (tall R wave) will be recorded.
Intrinsicoid Deflection
Intrinsic deflection: If a recording electrode is exper-
imentally placed directly over the epicardium of the left
ventricle, an R wave will be recorded because the ven-
tricles are activated from endocardium to epicardium.
The abrupt turnaround from the peak of the R wave
toward baseline is called the intrinsic deflection. It in-
dicates that the impulse has arrived at the site of the
recording electrode.

Depolarization and Repolarization Depolarization

of the Ventricles

Ventricular depolarization: The ventricles consist of

a thick layer of cells called the myocardium. The my-
ocardium can be divided arbitrarily into three layers
the endocardium, which is the inner layer; the mid-
myocardium or middle layer; and epicardium or outer
layer. Unlike the atria, the ventricles are depolarized by
special conduction pathways called the intraventricular
conduction system consisting of the bundle of His,
bundle branches, and fascicles. The intraventricular
conduction system terminates in a network of Purkinje
fibers, which are subendocardial in location. Depolar-
ization of both ventricles is synchronous and occurs
from endocardium to epicardium because the Purkinje
fibers are located subendocardially (Fig. 6.5). When the
ventricles are depolarized, a QRS complex is recorded.
If a recording electrode is placed on the chest wall
Purkinje fibers
-+
Endocardium
Epicardium
Figure 6.5: Depolarization of the Ventricles. Depolariza-
tion of the free wall of the ventricles starts from the endocardium
and spreads outward toward the epicardium (arrows) because the
Purkinje fibers are located subendocardially. A precordial lead
such as V5 will record a positive deflection because the electrode
is facing the positive end of the moving dipole.
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58 Chapter 6

A B R peak time: When there is intraventricular conduc-

R tion delay, the working group of the World Health Or-
Intrinsicoid ganization/International Society and Federation for
Deflection Cardiology prefers to use the term R peak time to indi-
R
cate the onset of the intrinsicoid deflection and is
measured from the onset of the QRS complex to the
peak of the R or R wave.
VAT R peak time

Figure 6.6: Intrinsicoid Deflection. (A) The ventricular

activation time (VAT) starts from the onset of the QRS complex
to the peak of the R wave. The intrinsicoid deflection is the
downward deflection that immediately follows the peak of the
R wave. (B) When there is bundle branch block, the R peak time is
the preferred terminology to identify the onset of the
intrinsicoid deflection and is measured from the onset of the
QRS complex to the peak of the R wave.
Intrinsicoid deflection: Clinically, the recording elec-
trode is normally placed on the chest wall and not di-
rectly over the epicardium. What is recorded is not the
intrinsic deflection, but its equivalent, the intrinsicoid
deflection. The time it takes for the impulse to arrive at
the recording electrode is the ventricular activation
time and is measured from the onset of the QRS com-
plex to the top of the R wave. The abrupt downward
deflection of the R wave that immediately follows is the
intrinsicoid deflection (Fig. 6.6). When there is right
ventricular hypertrophy, the onset of the intrinsicoid
deflection is delayed in right-sided precordial leads V1
or V2 (normal, 0.03 seconds). When there is left ven-
tricular hypertrophy, the onset of the intrinsicoid de-
flection is delayed in left sided precordial leads V5 or V6
(normal, 0.05 seconds).
The Normal Sequence of
Ventricular Activation
The normal QRS complex: When the conduction sys-
tem is intact, the sequence of ventricular activation oc-
curs in a predictable fashion that can be broken down
into three stages; vector 1 depolarization of the ventricu-
lar septum, vector 2 depolarization of the free walls of
both ventricles, and vector 3 depolarization of the poster-
obasal wall of the left ventricle and posterobasal septum.
Vector 1depolarization of the ventricular
septum: When the sinus impulse finally arrives at
the ventricles, the first portion of the ventricle to be
activated is the middle third of the left side of the
ventricular septum. This is because the left bundle
branch is shorter than right bundle branch. The sep-
tum is activated from left to right as represented by
the arrows in Figure 6.7A. Any electrode located to
the right of the ventricular septum (such as V1) will
record a positive deflection (small r wave) because
the impulse is traveling toward the positive side of
the electrode. Any electrode located to the left of the
septum (such as precordial leads V5, V6, and limb
leads I and aVL) will record a negative deflection
(small q wave) because the impulse is traveling away
from the positive side of these electrodes. This small

Superior
B Posterior
A
aVR aVL

LV R L R I L
1 V5 1

RV
V5, V6, V1 III II
aVF
I, aVL
Anterior Inferior
Horizontal Plane Frontal Plane
V1

Figure 6.7: Vector 1Initial Activation of the Ventricles. (A) The earliest portion of the ventricles to
be activated is the left side of the ventricular septum (arrow) at its mid-portion. The initial electrocardiogram
for V1 and for V5-6 or leads I and aVL are shown. (B) In the horizontal and frontal planes, the direction of the ini-
tial vector is represented by the arrows indicated by the number 1. This initial impulse is directed to the right,
anteriorly and inferiorly. LV, left ventricle; RV, right ventricle; R, right; L, left.
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Depolarization and Repolarization 59

q wave is often called septal q wave to indicate that are located superiorly in relation to the other struc-
the initial vector of the QRS complex is due to sep- tures of the heart. Thus, the late forces are directed
tal activation. The total duration of the normal sep- superiorly and posteriorly (Fig. 6.9).
tal q wave should not exceed 0.03 seconds. Vectors one through three are oversimplifications of
Vector 2depolarization of both ventricles: the complex process of ventricular depolarization and
Depolarization of the free wall of both ventricles oc- are summarized in Figure 6.10. These vectors differ
curs simultaneously, beginning within the endo- both spatially and temporally and produce a unique
cardium adjacent to the subendocardial Purkinje QRS complex that is contingent on the location of the
fibers and spreading outward toward the epi- recording electrode.
cardium. Activation of the remaining ventricular
septum occurs on both sides of the septum simulta-
neously, which cancels each other. Activation of the Ventricular Repolarization
free wall of both ventricles also occurs in opposite
directions, and similarly neutralizes one another.
Repolarization: Unlike the situation in the single
Because the right ventricle is thinner than the left
muscle cell or the atria where depolarization and repo-
ventricle, a certain portion of the forces generated
larization travel in the same direction, depolarization
by the thicker left ventricle will remain unopposed.
and repolarization of the ventricular myocardium oc-
Additionally, apical depolarization forces are not
cur in opposite directions. Thus, depolarization starts
neutralized because the area opposite the apex is oc-
from endocardium to epicardium (Fig. 6.11A) and re-
cupied by the non-muscular mitral and tricuspid
polarization is reverse, occurring from epicardium to
valves. Taken together, these two forces manifest in a
endocardium (Fig. 6.11B). This causes the QRS com-
vector 2 that is directed to the left and slightly poste-
plex and T wave to be inscribed in the same direction.
riorly, either inferiorly or superiorly, and corre-
Thus, precordial electrodes V5 and V6 will record a pos-
sponds to the mean axis of the QRS complex. A
itive deflection (tall R wave) during depolarization and
downward deflection (deep S) is recorded in V1 and
also a positive deflection during repolarization (up-
an upward deflection (tall R) is recorded in V5V6
right T wave) because these precordial electrodes are
(Fig. 6.8).
facing the positive end of the moving dipole.
Vector 3terminal portion of the QRS complex:
Several explanations have been offered as to why the
Depolarization of the ventricles occurs in an apex to
epicardial cells recover earlier than the endocardial
base direction. Thus, the last portion of the ventri-
cells even if they are the last to be depolarized. More re-
cles to become depolarized includes the poster-
cently, it has been shown that the action potential du-
obasal wall of the left ventricle and posterobasal
ration of endocardial cells is longer when compared
portion of the ventricular septum. These structures

A B Superior
Posterior
aVR aVL

V5 2
L R
R IL
LV 1 V5 1
2
RV
V1 III II
aVF
Anterior
V1 Inferior
Horizontal Plane Frontal Plane

Figure 6.8: Vector 2 or Depolarization of the Free Walls of Both Ventricles. (A) Both ventricles are
depolarized from endocardium to epicardium in an outward direction (small arrows). The mean direction of vec-
tor 2 is represented by the large arrow, which is toward the left, posteriorly and superiorly or inferiorly. (B) The
mean direction of vector 2 is shown in the horizontal and frontal planes. Vector 2 corresponds to the mean axis
of the QRS complex, which is 30 to 90 in the frontal plane. In the above example, the frontal plane vector is
close to 60 and is inferior. RV, right ventricle; LV, left ventricle; R, right; L, left.
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A B Posterior Superior

V5 aVR aVL
3 2 3 2 3
R L
1
LV
V5
2 3 R I 1
1 L
RV 1
2
V1 III II
Anterior aVF
V1 Inferior
Horizontal Plane Frontal Plane

Figure 6.9: Vector 3Terminal Portion of the QRS Complex. (A) The posterobasal portion of the sep-
tum and left ventricle are the last segments to be depolarized. The terminal vector is directed superiorly and pos-
teriorly. (B) The direction of vector 3 in the horizontal and frontal planes is shown. L, left; R, right; LV, left ventricle;
RV, right ventricle.

V5
V5
V5

V1 V1 V1

A B C

Figure 6.10: Summary of the Sequence of Ventricular Activation. The

initial vector (A) represents depolarization of the left side of the ventricular septum
at its mid-portion, which is directed to the right, anteriorly and inferiorly. (B) Vector
2 is directed to the left, posteriorly and superiorly or inferiorly corresponding to the
mean axis of the QRS complex. (C) Vector 3 is directed superiorly and posteriorly.

A. Depolarization B: Repolarization

-+
-+
Endocardium
Endocardium Epicardium
Epicardium

Figure 6.11: Ventricular Repolarization. (A) Diagram showing depolarization of

the ventricular myocardium, which starts from endocardium to epicardium.This causes
the QRS complex to be upright since the depolarization wave is advancing toward the
recording electrode. Arrows point to the direction of depolarization. (B) Repolarization of
the ventricular myocardium is from epicardium to endocardium. Because the repolariza-
tion wave is moving away from the recording electrode, the recording electrode is facing
the positive side of the moving dipole.Thus, a positive deflection (upright T wave) is
recorded. Arrows point to the direction of repolarization.

60
LWBK271-C06_55-61.qxd 29/1/09 10:09 pm Page 61 LWBK270-4119G-C02_073-110.qxd
with epicardial cells. This is most probably the main
reason why the epicardial cells recover earlier than en-
docardial cells causing repolarization to start from
epicardium to endocardium.
Depolarization and Repolarization
of the Atria and Ventricles
Depolarization and Repolarization
Single muscle cell: In a single muscle cell, depolarization
and repolarization travel in the same direction. Thus, the R
wave and the T wave are normally inscribed in opposite di-
rections. If the QRS complex is upright or positive, then
the T wave is normally inverted, and if the QRS is negative
or inscribed downward, then the T wave is normally
upright.
Atria: The direction of depolarization and repolarization of
the atria is similar to that of a single muscle cell. The sinus
impulse spreads longitudinally from right atrium to left
atrium. Repolarization occurs in the same direction. Thus, if
an electrode records an upright P wave, the repolarization or
Ta wave is inverted and if the electrode records an inverted P
wave, the Ta wave is upright.
Ventricles: Depolarization and repolarization of the ventri-
cles occur in opposite directions. Thus, if the QRS complex is
upright or positive, then the T wave is also upright. If the
QRS complex is negative, then the T wave is inverted.
Mechanism
Single muscle cell: In a single muscle cell, depolarization
and repolarization occur in the same direction because the
area that is first depolarized has had a longer time to recover.
Atria: The atria consist of a thin layer of cells. Unlike the ven-
tricles, the atria do not have a special conducting system.
Thus, the impulse is spread from one muscle cell to the next
muscle cell longitudinally until both atria are depolarized.
Depolarization and repolarization is similar to a single mus-
cle cell and occur in the same direction.
Ventricles: The ventricles consist of a thick layer of muscle
cells and are depolarized from endocardium to epicardium
Depolarization and Repolarization 61
because the Purkinje fibers are located subendocardially. Un-
like the atria and the single muscle cell where depolarization
and repolarization occur in the same direction, depolariza-
tion and repolarization of the ventricles occur in opposite di-
rections. The reason as to why the epicardial cells recover ear-
lier than the endocardial cells despite being the last to be
depolarized may be due to the following reasons.
The endocardial cells have longer action potential dura-
tion compared with epicardial cells.
Myocardial perfusion occurs mainly during diastole when
the ventricles are relaxed and the pressures within the cav-
ities are lowest. Because repolarization (T wave) occurs
during systole when the myocardium is mechanically
contracting, there is no significant myocardial perfusion
within the subendocardial layer because it is subjected to
a much higher tension than the epicardium.
The endocardium has a higher rate of metabolism as
compared with the epicardium and thus requires more
oxygen than the epicardium.
The subendocardial layer is the deepest part of the my-
ocardium. Because the coronary arteries are anatomically
epicardial in location, the subendocardial areas are the far-
thest from the coronary circulation, making the endo-
cardium relatively ischemic as compared with the epi-
cardium.
Suggested Readings
Burch GE, Winsor T. Principles of electrocardiography. In: A
Primer of Electrocardiography. 5th ed. Philadelphia: Lea &
Febiger; 1966;166.
Dunn MI, Lipman BS. Basic physiologic principles. In: Lipman-
Massie Clinical Electrocardiography. 8th ed. Chicago: Year-
book Medical Publishers; 1989;2450.
Marriott HJL. Genesis of the precordial pattern. In: Practical
Electrocardiography. 5th ed. Baltimore: Williams & Wilkins
Co.; 1972;4455.
Sgarbossa EB, Wagner GS. Electrocardiography. In: Topol EJ ed.
Textbook of Cardiovascular Medicine. 2nd ed. Philadelphia:
Lippincott Williams & Wilkins; 2002:13301383.
Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for
intraventricular conduction disturbances and pre-excita-
tion. J Am Coll Cardiol. 1985;12611275.
LWBK271-C07_62-79.qxd 29/1/09 8:55 pm Page 62 LWBK270-4119G-C02_073-110.qxd
7
Chamber Enlargement
and Hypertrophy
The Normal P Wave
Normal sinus rhythm: The sinus node is the origin of
the normal impulse. The normal sinus P wave has the
following features.
Frontal plane:
n Axis: The axis of the normal P wave is approxi-
mately 45 to 60. Thus, the P wave is upright in
lead II. This is the most important lead in recog-
nizing that the rhythm is normal sinus. If the P
wave is not upright in lead II, the P wave is prob-
ably ectopic (not of sinus node origin).
n Contour: The normal P wave is smooth and well
rounded and should not be peaked or notched.
n Amplitude: The normal P wave is 2.5 mm in
height.
n Duration: The normal P wave is 2.5 mm wide
or 100 milliseconds in duration.
Horizontal plane:
n Sinus P waves are normally upright in V3 to V6. In
V1 and often in V2, the contour of the normal P
wave may be upright, inverted or biphasic. Biphasic
means that the initial portion of the P wave is up-
right and the terminal portion is inverted (Fig. 7.1).
The Normal Sinus P Wave
Lead II Lead V1
Upright Upright Biphasic Inverted
Figure 7.1: The Normal P Wave. The sinus P wave is well
rounded and smooth and is upright in leads I, II, and aVF meas-
uring 2.5 mm in height and 2.5 mm in width. In V1, a normal
P wave can be upright, biphasic, or inverted.
62
The inverted portion should measure 1 mm in
duration and 1 mm in depth.
Right Atrial Enlargement
Right atrial enlargement: The following changes oc-
cur when there is right atrial enlargement.
Frontal plane:
n Axis: The axis of the P wave is shifted to the right
of 60. Thus, the P waves are tall in leads II, III,
and aVF. The P waves in lead III are usually taller
than in lead I (P3  P1).
n Contour: The contour of the P wave is peaked
and pointed. These changes are often described
as P-pulmonale because right atrial enlarge-
ment is frequently caused by pulmonary disease.
n Amplitude: The height or amplitude of the P
wave increases to 2.5 mm. These P wave changes
are best seen in leads II, III, and aVF (Fig. 7.2).
n Duration: The total duration of the P wave is not
prolonged unless the left atrium is also enlarged.
Because the right atrium is activated earlier than
Right Atrial Enlargement
Leads II, III or aVF Lead V1
>2.5 mm
P-pulmonale Upright or Biphasic or Inverted P Waves
Figure 7.2: Right Atrial Enlargement. In right atrial
enlargement, the P waves are peaked and tall with an amplitude
2.5 mm in leads II, III, or aVF. Changes in V1 are less obvious,
although the upward deflection is often peaked. The duration
of the P wave is not widened.
LWBK271-C07_62-79.qxd 29/1/09 8:55 pm Page 63 LWBK270-4119G-C02_073-110.qxd
P Electrocardiogram of Right Atrial
S
RA 1
L R LA L
R L RA
2
I
A
Frontal Plane Horizontal Plane
Figure 7.3: Right Atrial Enlargement. In the frontal plane,
the right atrium enlarges downward and to the right causing a
shift in the P wave axis to the right (from arrow 1 to arrow 2). In
the horizontal plane, the enlargement of the right atrium is
slightly anterior, which may cause slight peaking of the P waves
in lead V1. The shaded portion indicates the changes that occur
when the right atrium enlarges. S, superior; I, inferior; R, right; L,
left; A, anterior; P, posterior; RA, right atrium; LA, left atrium.
the left atrium, any delay in the propagation
of the impulse from enlargement of the right
atrium will coincide with the activation of the
left atrium.
Horizontal plane: In V1, there may not be any sig-
nificant P wave changes. The P wave remains nor-
mally upright, biphasic, or inverted. The initial up-
right portion may be slightly peaked or pointed or it
might be slightly taller than normal.
When there is right atrial enlargement, the right atrium
enlarges downward and to the right, thus the axis of the
P wave is shifted vertically to the right of 60 (Fig. 7.3).
This causes the P wave in lead III to be taller than the P
wave in lead I.
II III aVF
Chamber Enlargement and Hypertrophy 63
Enlargement
1. The P waves are tall and peaked measuring 2.5 mm in leads
II, III, or aVF (Fig. 7.4).
2. The duration of the P wave is not increased unless the left
atrium is also enlarged.
Mechanism
Normal sinus P waves: The sinus node is located at the
right upper border of the right atrium near the entrance of
the superior vena cava. The sinus impulse has to spread from
right atrium to left atrium downward in a right-to-left direc-
tion. The initial portion of the P wave represents right atrial
activation and the terminal portion, left atrial activation. In
the frontal plane, the normal P wave axis is approximately
45 to 60 and is upright in leads I, II, and aVF. The tallest
P wave is usually recorded in lead II and the amplitude of the
normal P wave is 2.5 blocks. In V1, the normal sinus P wave
can be upright, biphasic, or inverted. The normal cutoff for
the total duration varies among different authors. The World
Health Organization/International Society and Federation of
Cardiology Task Force define the normal duration as 110
milliseconds, which is not easy to measure in the electrocar-
diogram (ECG). A width of 2.5 small blocks (100 mil-
liseconds) will be used as the normal P wave duration in this
text.
Right atrial enlargement: The right atrium enlarges
downward and to the right causing the direction of the sinus
impulse to slightly shift to the right of 60. This causes the
P waves to be taller and more peaked in leads II, III, and aVF.
Thus the P wave in lead III is usually taller than the P wave in
lead I (P3  P1). In V1 and V2, the initial portion of the P
wave may increase in amplitude, although the terminal
V1 Figure 7.4: Right Atrial En-
largement. Twelve-lead elec-
trocardiogram showing right
atrial enlargement. Tall and
peaked P waves, also called P-
pulmonale, are seen in leads II,
III, and aVF (arrows). Note that
the P waves are taller in lead III
than in lead I. Leads II, III, aVF, and
V1 are magnified to show the ab-
normal P wave contour. The pa-
tient has chronic obstructive pul-
monary disease.
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64 Chapter 7

portion representing left atrial activation is not affected.
Because the right atrium is activated earlier than the
left atrium, any delay in activation of the atria due to en-
largement of the right atrium will coincide with activation
of the left atrium. Thus, the duration of the P wave is not
prolonged.
Clinical Implications
Enlargement of the right or left atrium occurring inde-
pendently is rare. It is usually associated with disease of the
valvular structures or the ventricles. The most common
cause of right atrial enlargement without left atrial enlarge-
ment in the adult population is pulmonary disease. Thus,
the tall, narrow, and peaked P wave of right atrial enlarge-
ment is often described as P-pulmonale. Right atrial en-
largement can be due to tricuspid or pulmonary valve dis-
ease, pulmonary hypertension, acute pulmonary embolism,
and right ventricular failure or hypertrophy from varied
causes.
Enlargement of either atria predisposes to atrial arrhyth-
mias, especially atrial flutter or atrial fibrillation. It is
uncommon for atrial flutter or fibrillation to become sus-
tained and self-perpetuating unless the atria are enlarged or
diseased.
When the lungs are hyperinflated because of emphysema,
the diaphragm is pushed downward. The right atrium may
also be displaced downward. When this occurs, the P wave
in V1 may become totally inverted because the diaphragm
and the heart are pushed vertically downward while the
standard location of the V1 electrode remains unchanged
at the 4th intercostal space to the right of the sternum. The
inverted P wave may be mistaken for an enlarged left
atrium.
Right atrial enlargement is due to volume or pressure
overload within the right atria. This causes the right atrial
size to increase. Right atrial enlargement is recognized at
bedside by the presence of distended neck veins. When the
patient is semirecumbent at an angle of 45, and the neck
veins are distended above the clavicle, the pressure in the
right atrium is elevated.
Treatment and Prognosis
The treatment and prognosis of right atrial enlargement will
depend on the etiology of the right atrial enlargement.
Left Atrial Enlargement
Left atrial enlargement: The ECG changes of left
atrial enlargement are best reflected in the terminal
half of the P wave because the right atrium is activated
earlier than the left atrium. The ECG features of left
atrial enlargement are summarized in Figure 7.5.
Frontal plane:
n Axis: The axis of the P wave is shifted to the left,
thus the P waves are taller in lead I than in lead
III (P1  P3).
n Contour: The contour of the P wave is bifid or
M shaped. The first hump represents activa-
tion of the right atrium and the second hump
represents activation of the left atrium. These
two humps are separated by at least one small
block and are best seen in leads I, II, aVF, V5, and
V6. This type of P wave is often called P-mitrale,
indicating that at some time in the past, mitral

Left Atrial Enlargement

Leads I, II or aVF Lead V1

>1 mm >1 mm
>2 mm

>1 mm >1 mm

P-mitrale Terminally inverted Totally Inverted

Figure 7.5: Left Atrial Enlargement. The duration of the P wave is prolonged meas-
uring 2.5 mm in leads I, II, or aVF, with a bifid or M-shaped configuration. This type of
P wave is called P-mitrale. In lead V1, the P wave may be totally inverted or it may be
biphasic. The inverted portion is broad and deep measuring 1 mm wide and 1 mm
deep.
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Chamber Enlargement and Hypertrophy 65

stenosis is the most common cause of left atrial P

enlargement.
n Amplitude: The height or amplitude of the P
wave is not significantly increased.
n Duration: The duration or width of the P wave is
increased and should measure 2.5 mm (100
milliseconds).
Horizontal plane:
n In lead V1, the P wave is biphasic or inverted. The
inverted portion measures 1 mm in depth and
1 mm (0.04 seconds) in duration.
The left atrium enlarges to the left and posteriorly shift-
ing the P wave axis to the left of 45. The P wave ab-
normalities are best seen in leads I, II, aVF and V1 (Figs.
7.6 and 7.7).
Bi-Atrial Enlargement
Bi-atrial enlargement: When both atria are enlarged,
the criteria for right atrial and left atrial enlargement
are both present because the atria are activated sepa-
rately (Fig. 7.8).
Frontal plane: In the frontal plane, the P waves
are tall measuring 2.5 mm because of right atrial
S
R RA LA L R L
LA
I
RA
A
Frontal Plane Horizontal Plane
Figure 7.6: Left Atrial Enlargement. The left atrium en-
larges to the left and posteriorly. Because activation of the atria
is sequential, starting from right atrium to left atrium, the dura-
tion of the P wave is prolonged. The P waves are not only wide
but are notched in leads I, II, and aVF. The terminal portion is in-
verted in lead V1. S, superior; I, inferior; R, right; L, left; A, anterior;
P, posterior; RA, right atrium; LA, left atrium.
enlargement. At the same time, the P waves are
broad, notched, or M-shaped measuring 2.5 mm
wide from left atrial enlargement. These changes
are best seen in leads I, II, and aVF (Fig. 7.9).
Horizontal plane: In the horizontal plane, the P wave
in V1 is biphasic or inverted. The initial positive por-
tion is usually peaked due to right atrial enlargement

I II V1

aVF

Figure 7.7: Left Atrial Enlargement. The P waves are wide in leads I, II, III, and aVF as well as several other
leads. The configuration of the P wave is M-shaped (P-mitrale). The P wave is negative in V1. The negative deflection
measures at least 1  1 (1 mm wide and 1 mm deep).
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66 Chapter 7

Bi-atrial Enlargement

Leads II, III or aVF Lead V1

>2.5 mm >1 mm
>2.5 mm
>1
mm
>2.5 mm >2.5 mm >1 mm >1 mm

Figure 7.8: Bi-atrial Enlargement. Bi-atrial enlargement is characterized by tall and

broad P waves measuring 2.5 mm in height and 2.5 mm in duration. In V1, the P wave is
biphasic or inverted. The initial portion may be peaked due to right atrial enlargement. The
inverted portion is broad and deep measuring 1 mm wide and 1 mm deep because of left
atrial enlargement.

and the terminal negative portion is 1 mm wide
and 1 mm deep from left atrial enlargement.
Intra-Atrial Block
Intra-atrial block: According to an ad hoc working
group organized by the World Health Organization
and International Society and Federation in Cardi-
ology, the P wave duration should not exceed 0.11
seconds in the adult. The normal cutoff for the P
wave duration, however, varies among authors. In-
creased duration of the P wave implies that there is
intra-atrial block that may be due to left atrial en-
largement but can also be caused by scarring or fi-
brosis of the atria.
Left atrial enlargement: In left atrial enlargement, the P
wave duration is always prolonged because of intra-atrial
block or prolonged atrial conduction. Increased left atrial
pressure or volume is not always present. Thus, left atrial
abnormality may be a better terminology to describe the P
wave changes associated with left atrial enlargement.
A 12-lead ECG is shown in Figure 7.10. The P waves are
notched with an M-shape configuration in lead II. The P
wave measures 2.5 mm wide with both peaks separated
by one small block. The configuration of the P wave is
consistent with P-mitrale. The P wave in V1 is not deep
or wide. Although there is intra-atrial block, not all the P
wave changes satisfy the criteria for left atrial enlargement.

Figure 7.9: Electrocardiogram of Bi-atrial Enlargement. The P waves are peaked and wide. In leads II and
aVF, the P waves are 2.5 mm tall and 2.5 mm wide (100 milliseconds in duration). In V1, the P waves are termi-
nally negative and are 1 mm wide and 1 mm deep.
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Lead II
Figure 7.10: Intra-atrial Block. Any sinus P wave that is prolonged, measuring 2.5 blocks is intra-atrial block.
This could be due to left atrial enlargement, but could also be due to other causes. Leads II and V1 are enlarged so
that the P waves are better visualized.
Left Atrial Enlargement
ECG of Left Atrial Enlargement
1. The duration of the P wave is increased in leads I, II, or aVF.
The P waves are often notched with M shape pattern meas-
uring 2.5 mm in width or 100 milliseconds in duration.
2. Terminally inverted P waves in V1 measuring 1 mm in depth
and 1 mm in duration.
Mechanism
When there is left atrial enlargement, the initial portion of the
P wave representing right atrial activation is not altered. The
terminal portion representing left atrial activation becomes
longer, resulting in a broader P wave. Thus, the total duration
of the P wave is prolonged. The general direction of the P wave
is slightly altered becoming more horizontal at 20 to 40.
Thus, the P wave in lead I is taller than the P wave in lead III (P1
 P3). The P wave abnormalities are best seen in lead II and of-
ten in leads I and aVF and precordial leads V5 and V6. The P
wave is frequently bifid with two separate humps, at least 0.04
seconds apart. The first hump represents right atrial activation
Chamber Enlargement and Hypertrophy 67
Lead V1
and the second hump represents activation of the enlarged
left atrium. Because mitral valve disease is a common cause
of left atrial enlargement, the notched and M-shaped P wave
of left atrial enlargement is described as P-mitrale.
Because the left atrium is oriented to the left and posterior to
that of the right atrium, an enlarged left atrium will cause the
terminal forces of the P wave to be directed to the left and
posteriorly. In V1, the terminal portion, which represents left
atrial activation, will be oriented more posteriorly than nor-
mal, causing the P wave to be broad and deep measuring at
least 1 mm wide and 1 mm deep equivalent to one small box.
Clinical Significance
Primary disease involving the left atrium alone is rare. Enlarge-
ment of the left atrium, therefore, is secondary to abnormalities
involving the mitral valve or the left ventricle including mitral
stenosis or insufficiency, left ventricular systolic, or diastolic
dysfunction from several causes such as hypertension, coronary
artery disease, cardiomyopathy, and aortic valve disease.
Left atrial enlargement is a common finding in patients with left
ventricular hypertrophy (LVH). The presence of left atrial en-
largement is one of the criteria for the ECG diagnosis of LVH.
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68 Chapter 7
Because the atria are activated circumferentially, and the elec-
trical impulse travels through the length of the atrial wall, en-
largement is preferred over hypertrophy when describing
the presence of atrial enlargement. The P wave changes in the
ECG do not reflect thickening or hypertrophy of the atrial
wall, but rather, increase in the dimension of the atrial cavity
or prolonged conduction in the atria from intra-atrial block.
Additionally, when pulmonary hypertension occurs from pul-
monary embolism or heart failure, the P wave changes can oc-
cur acutely. It can also regress acutely when the pulmonary
pressure resolves, which is unlikely if the changes are due to
atrial hypertrophy. This is in contrast to the ventricles, where
electrical activation is from endocardium to epicardium. The
changes in the QRS complex represent increased left ventricu-
lar mass or thickness. Thus, either enlargement or hypertro-
phy is appropriate in describing the increased ventricular
mass, whereas atrial enlargement or atrial abnormality is more
appropriate in describing the changes in the atria.
Treatment and Prognosis
Left atrial enlargement is most often associated with abnor-
malities of either the mitral valve or left ventricle. The treat-
ment and prognosis will depend on the underlying cause of
the left atrial enlargement.
Left Ventricular Hypertrophy
LVH: The sensitivity of the ECG in detecting LVH is
limited; thus, several criteria have been proposed. Most
of these ECG abnormalities are based on increased
voltage of the QRS complex from increased mass of the
Figure 7.11: Left Ventricular Hypertrophy. Twelve-lead electrocardiogram showing left ventricular hypertro-
phy. The P wave in V1 is 1 mm wide and 1 mm deep because of left atrial enlargement. The voltage of the QRS com-
plex is increased with deep S waves in V1 and tall R waves in V5 and V6. ST depression with T wave inversion is present
in leads with tall R waves (LV strain).
left ventricle when there is LVH. These changes include
the following (see Figs. 7.11 and 7.12).
Abnormalities in the QRS complex
n Deep S waves in V1 or V2 measuring 30 mm
n Tall R waves in V5 or V6 measuring 30 mm
n S in V1  R in V5 or V6 35 mm
n Tall R waves in aVL measuring 11 mm
n Tall R or deep S in any limb lead 20 mm
n R in aVL  S in V3 28 mm (men) and 20 mm
(women)
n The total amplitude of the QRS complex exceeds
175 mm in all 12 leads
n Onset of intrinsicoid deflection 0.05 seconds
in V5 or V 6
n Increased duration of the QRS complex 0.09
seconds
n Left axis deviation 30
Abnormalities in the P wave
n Left atrial abnormality
Abnormalities in the ST segment and T wave
n ST depression and T inversion in leads with tall R
waves (left ventricular strain)
Increased voltage of the QRS complex: The voltage
of the QRS complex is increased when there is LVH.
Unfortunately, the amplitude of the QRS complex may
not be a reliable marker of LVH because it can be al-
tered by several factors other than increased thickness
of the left ventricular wall.
LVH without increased voltage: Patients with
LVH may not exhibit any increase in QRS voltage
because of obesity, peripheral edema, anasarca,
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Chamber Enlargement and Hypertrophy 69

Lead V1 Left Ventricular

Figure 7.12:
Left atrial
abnormality Hypertrophy. Diagrammatic
representation of the different
electrocardiogram changes in left
Deep S in V1 or V2 ventricular hypertrophy.
Lead aVL
Delayed onset of
intrinsicoid deflection
R wave in aVL
>0.05 second
>11 mm
Tall R in V5 or V6
Left axis
0
deviation -30
Slight widening of the
QRS complex
Left ventricular strain

P-mitrale
Lead V5 or V6
S in V1 + R in V5 or V6 = >35 mm

increased diameter of the chest, lung disease espe-
cially emphysema, large breasts, biventricular hyper-
trophy, amyloidosis, pericardial effusion, pleural
effusion, and hypothyroidism.
Increased voltage not resulting from LVH: Con-
versely, increased voltage of the QRS complex may be
present even in the absence of LVH in adolescent boys,
anemia, left mastectomy, and in thin individuals.
Left atrial abnormality: Enlargement of the left
atrium is included as one of the diagnostic hallmarks of
LVH. During diastole when the mitral valve is open, the
left atrium and left ventricle behave as a common
chamber. Thus, changes in pressure and volume in the
left ventricle are also reflected in the left atrium.
Ventricular activation time: Ventricular activation
time represents the time it takes for the ventricular im-
pulse to arrive at the recording electrode and is measured
from the onset of the QRS complex to the top of the R or
R wave (Fig. 7.13A, B). The thicker the myocardium, the
longer it takes for the impulse to travel from endo-
cardium to epicardium. Thus, when there is LVH, the
ventricular activation time of leads overlying the left ven-
tricle (V5 or V6) is prolonged (0.05 seconds).
Intrinsicoid deflection: The intrinsicoid deflection
corresponds to the time that the depolarization wave
has arrived at the recording electrode and is repre-
sented by the sudden downward deflection of the R
wave toward baseline. If there is LVH, the onset of the

A B VAT
Onset of
VAT > 0.05 second intrinsicoid
deflection

V6
V1
Intrinsicoid
deflection Endocardium

VAT
Precordial
Electrode

Ventricular Activation Time (VAT) Epicardium

Figure 7.13: Intrinsicoid Deflection. The ventricular activation time (VAT) is

measured from the onset of the QRS complex to the top of the R wave. The intrinsicoid de-
flection is represented by the immediate downward deflection of the R wave toward base-
line (A). When there is left ventricular hypertrophy, the onset of the intrinsicoid deflection
(dotted lines in A and B) is delayed in V5 or V6. When there is right ventricular hypertrophy,
the onset of the intrinsicoid deflection is delayed in V1 or V2.
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70 Chapter 7
intrinsicoid deflection in leads V5 or V6 is delayed (Fig.
7.13B).
Abnormalities in the ST segment and T wave: Be-
cause depolarization of the left ventricle is abnormal,
repolarization is also abnormal resulting in ST segment
depression and T wave inversion in leads with tall R
waves. Left ventricular strain is frequently used to de-
scribe this pattern of ST depression and T wave inver-
sion (Fig. 7.12).
LVH is a compensatory mechanism in response to both
pressure and volume overload.
Pressure overload: LVH from pressure overload is
usually due to systemic hypertension, aortic steno-
sis, coarctation of the aorta, or hypertrophic ob-
structive cardiomyopathy. When there is pressure or
systolic overload, the left ventricle becomes concen-
trically hypertrophied. The walls of the left ventricle
are thickened although the size of the left ventricu-
lar cavity remains normal. The ECG shows tall R
waves in V5 and V6 associated with depression of the
ST segment and inversion of the T wave. These ST-T
changes are often described as due to left ventricular
strain (Figs. 7.11 and 7.12).
Volume overload: This type of LVH is due to in-
creased volume of the left ventricle as would occur
when there is mitral regurgitation, aortic regurgita-
tion, ventricular septal defect, peripheral arteriove-
nous shunts, anemia, and thyrotoxicosis. When
there is volume or diastolic overload, the left ventri-
cle becomes eccentrically hypertrophied. The left
ventricular cavity becomes dilated. There is also in-
creased left ventricular mass. The ECG shows
prominent Q waves, tall R waves, and tall and up-
right T waves in V5 and V6 (Fig. 7.14).
Figure 7.14: Left Ventricular Hypertrophy from Volume Overload. Twelve-lead electrocardiogram (ECG)
showing tall voltage measuring 45 mm in V5 and 25 mm in V6 combined with prominent Q waves and tall T
waves. This pattern of LVH is usually due to volume overload. This ECG is from a 55-year-old man with sickle cell
anemia with gross cardiomegaly by chest x-ray.
LVH associated with left ventricular strain is more
common than LVH from volume overload because hy-
pertension is the most common cause of LVH.
The ECG of LVH
Several ECG criteria have been used in the diagnosis of LVH.
These include:
Increased amplitude or voltage of the QRS complex
n Limb leads
n R wave in any limb lead measuring 20 mm
n S wave in any limb lead measuring 20 mm
n R wave in aVL 11 mm
n R in lead I  S in III 25 mm
n Precordial leads
n S wave in V1 or V2 30 mm
n R wave in V5 or V6 30 mm
n R wave in V5 or V6 26 mm
n S wave in V1, V2 or V3 25 mm
n R wave in V4, V5 or V6 25 mm
n SV1  RV5 or V6 35 mm
n Tallest S  tallest R in V1 to V6 45 mm
n R wave in V6  R wave in V5
n Limb  Precordial leads
n R wave in aVL  S wave in V3 20 mm in females
n R wave in aVL  S wave in V3 28 mm in males
n Total QRS voltage from all 12 ECG leads 175 mm
Increased duration of the QRS complex
n Delayed onset of intrinsicoid deflection 0.05 sec-
onds in V5 or V6
n Increased duration of the QRS complex 0.09 seconds
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Chamber Enlargement and Hypertrophy 71

Left atrial abnormality endocardium to epicardium. These forces occur in opposite di-
n Terminal negativity of the P wave in V1 measuring rections and cancel out. Because the left ventricle is normally
1 mm  1 mm thicker than the right ventricle, the left ventricle continues to
Left axis deviation undergo electrical activation even after activation of the right
n 30
ventricle is completed. Therefore, activation of the left ventricle
continues unopposed. This vector corresponds to the main axis
n 15
of the QRS complex and is oriented to the left and posteriorly.
ST-T abnormalities indicating left ventricular strain Tall R waves are normally recorded in leads V5-6 and deep S
in V5 or V6 waves are recorded in lead V1 and often in V2. When there is left
n ST segment depression ventricular hypertrophy, these findings become exaggerated.
n T wave inversion The R waves become taller in left sided leads V5, V6, and aVL.
The following are the criteria that are frequently used in the di- Right-sided chest leads such as V1 and V2, will record deep S
agnosis of LVH. waves. When there is respiratory variation, the largest deflec-
Sokolow-Lyon Index: This is the most commonly used cri- tion is selected to represent the magnitude of the QRS complex.
teria for the diagnosis of LVH. Pressure overload: LVH from increased systolic pres-
R in V5 or V6  S in V1
35 mm sure can occur when there is aortic or subaortic obstruc-
tion or when there is systemic hypertension. This type of
R in aVL 11 mm
LVH is often called pressure overload or systolic overload
Romhilt and Estes:
and is usually characterized by the presence of a thick left
3 points each ventricle with normal cavity dimension. R waves are tall
n P wave from left atrial abnormality in the left sided chest leads V5 or V6 and deep S waves are
n Any increase in voltage of the QRS complex present in right-sided chest leads V1 or V2. The ST seg-
n R or S in limb lead
20 mm ments are depressed and T waves are inverted in leads
n S in V1 or V2
30 mm
with tall R waves. These ST-T abnormalities are fre-
quently described as left ventricular strain. This type of
n R in V5 or V6
30 mm
LVH is associated with a high systolic pressure.
n ST-T abnormalities
Volume overload: LVH can also be due to volume over-
n Any shift in the ST segment (without digitalis)
3
load such as valvular regurgitation, ventricular septal defect,
2 points patent ductus arteriosus, and other extracardiac left-
n Left axis deviation of 30 to-right shunts. This type of LVH is often called volume
1 point each overload or diastolic overload and is usually characterized
n Slight widening of the QRS complex of 0.09 seconds by the presence of a dilated left ventricular cavity. Promi-
nent Q waves are present in leads with tall R waves such as
n Intrinsicoid deflection in V5 or V6 of 0.05 seconds
V5 and V6 accompanied by tall rather then inverted T waves.
n ST-T abnormalities with digitalis
Left atrial abnormality: LVH is frequently associated with
Score of 5 points
LVH; score of 4 points
probable LVH
enlargement of the left atrium. When there is LVH, there is
Cornell voltage criteria:
increased left ventricular end diastolic pressure or volume.
R in aVL  S in V3
28 mm in men and 20 mm in This will also increase left atrial pressure or volume because
women. the left atrium and left ventricle behave as common chamber
Cornell product: when the mitral valve is open during diastole.
Cornell voltage multiplied by the QRS duration in mil- Prolonged ventricular activation time: The ventricular
liseconds
2,440 milliseconds. (In women, 6 mm is activation time represents the time it takes for the impulse to
added to Cornell voltage.) activate the myocardium below the recording electrode. The
Total QRS voltage: thicker the myocardium, the longer it takes for the electrical
Total QRS voltage or total amplitude of the QRS complex impulse to travel from endocardium to epicardium. This is
obtained from all 12 leads. The normal voltage averages measured from the onset of the QRS complex to the top of
129 mm (range, 80 to 185 mm) with 175 mm as the upper the R wave. Thus, the electrodes overlying the left ventricle,
limits of normal. such as leads V5 or V6, will record a longer ventricular activa-
tion time of 0.05 seconds when there is LVH.
Delayed onset of the intrinsicoid deflection: The intrinsi-
Mechanism
coid deflection represents that moment in time that the im-
Increased voltage of the QRS complex: Increased voltage pulse has reached the epicardium and is represented as a down-
of the QRS complex is frequently used as one of the criteria ward deflection of the R wave toward baseline. The onset of the
for LVH. When the ventricles are activated, the free walls of intrinsicoid deflection signals that the whole myocardium
both ventricles (vector 2) are activated simultaneously from below the recording electrode has been fully activated. Because
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72 Chapter 7
the ventricular activation time is prolonged when there is LVH,
the onset of the intrinsicoid deflection in V5 or V6 is also de-
layed.
Increased duration of the QRS complex: When there is
LVH, left ventricular mass is increased; thus, activation of the
left ventricle will take longer. When LVH is present, the dura-
tion of the QRS complex is increased. The QRS is widened
not only because of the increased muscle mass or increased
ventricular activation time but intraventricular conduction
delay may be present.
Left axis deviation 30: Left axis deviation may occur
when there is LVH because of increased muscle mass result-
ing in a more horizontal axis of the QRS complex. Addition-
ally, LVH is frequently associated with left anterior fascicular
block or incomplete left bundle branch block, which can
shift the QRS axis more markedly to the left.
ST and T wave abnormalities: The ST segment and T wave
represent ventricular repolarization corresponding to phases
2 and 3 of the transmembrane action potential, respectively.
Normally, when the ventricles are activated, repolarization
begins immediately. During phase 2, corresponding to the ST
segment, the electrical potential is normally maintained at
almost 0 potential for a sustained duration; thus, there is no
deflection recorded in the ECG. The T wave is inscribed only
when sufficient potential is generated during repolarization
corresponding to the down slope or phase 3 of the trans-
membrane action potential.
ST depression: When there is LVH, ventricular activa-
tion is prolonged. Repolarization begins in some areas of
the ventricle even before the whole myocardium is com-
pletely depolarized. This allows repolarization to occur
relatively earlier than usual, which can reach sufficient
magnitude to cause downward deviation of the ST seg-
ment in leads with tall R waves.
T wave inversion: The T wave in LVH is inverted and is op-
posite in direction to that of the QRS complex. This implies
that depolarization and repolarization of the myocardium
occur in the same direction, which is the opposite of nor-
mal. The prolonged activation time of the thickened left
ventricle allows the endocardium to recover earlier even be-
fore the whole thickness of the myocardium is completely
depolarized. Thus, repolarization proceeds from endo-
cardium to epicardium, resulting in depression of the ST
segment and inversion of the T waves in leads with tall R
waves. Additionally, when the left ventricle is thickened, the
myocardium may outstrip its normal blood supply even in
the absence of occlusive coronary disease. Thus, the whole
thickness of the left ventricle becomes relatively ischemic.
The endocardium, which is the first to be depolarized, will
recover earlier because it had a longer time to recover.
Clinical Significance
Although LVH is a physiologic response to pressure or vol-
ume overload, it is a marker of increased cardiovascular
morbidity and is a known risk factor for sudden cardiovas-
cular death. The presence of LVH may be a predictor of LV
dysfunction within 5 years after its detection.
Hypertension is the most common cause of LVH. In hyper-
tensive patients, LVH occurs as a compensatory adaptation
from pressure overload. LVH due to hypertension can
regress with antihypertensive medications. All antihyper-
tensive medications are generally effective in regressing LVH
except hydralazine and minoxidil. There is clinical evidence
to show that regression of LVH in patients with hyperten-
sion reduces cardiovascular events. A baseline ECG there-
fore is standard examination in patients initially diagnosed
with hypertension.
The several ECG criteria proposed for the diagnosis of LVH
suggest that none of these criteria is optimal. The sensitivity
of the ECG in diagnosing LVH is relatively poor and is
50%. However, when LVH is diagnosed by ECG, the speci-
ficity is high and is approximately 90%. The diagnosis of
LVH in the ECG is primarily dependent on the presence of
increased voltage. Unfortunately, voltage can be affected by
many conditions other than LVH. The echocardiogram is
more sensitive and more specific than the ECG for the de-
tection of LVH, but is less readily available and much more
expensive. The ECG remains the procedure of choice and is
the most important modality in detecting LVH in patients
with hypertension.
When there is LVH, physical examination will show the fol-
lowing findings:
Normal apical impulse: The apex of the heart is nor-
mally occupied by the left ventricle. The apex impulse,
which is the lowest and most lateral cardiac impulse in the
precordium, is due to left ventricular contraction and
normally occupies 2 cm (the size of a quarter) and con-
fined to only one intercostal space. In some patients, the
apex impulse may not be palpable.
Concentric LVH: When the left ventricle is concentrically
hypertrophied, the left ventricular cavity is not enlarged
and the apex impulse is not displaced. The area occupied
by the apex impulse, however, becomes wider measuring
about 2 to 3 cm or more in diameter, thus occupying an
area that may involve two intercostal spaces. Further-
more, the apex impulse becomes more sustained and
longer in duration compared with the short precordial
tap that is normally expected when the left ventricle is not
hypertrophied. A prominent 4th heart sound is usually
audible if the patient is in normal sinus rhythm, which
may be palpable as a prominent outward pulsation at the
apex before systole. This is better appreciated when the
patient is lying in lateral decubitus position.
Eccentric LVH: When there is eccentric LVH, the left ven-
tricular cavity is dilated. The apex impulse is displaced
laterally and downward and may reach the 6th or 7th in-
tercostal space at the left anterior axillary line. The pre-
cordial impulse becomes more diffuse involving a wider
area in the precordium.
LWBK271-C07_62-79.qxd 29/1/09 8:55 pm Page 73 LWBK270-4119G-C02_073-110.qxd
Figure 7.15: Right Ventricular Hypertrophy. There is right axis deviation, the QRS complexes are tall in V1 and
P waves are peaked in II and aVF. This pattern of right ventricular hypertrophy is described as type A and is frequently
seen in severe right ventricular hypertrophy often associated with congenital heart disease or severe mitral stenosis.
Treatment and Prognosis
LVH detected by ECG is a risk factor for increased cardiovas-
cular death. When ECG changes of LVH occur, the risk for
cardiovascular morbidity and mortality increases, and the
risk is even higher when ST and T wave abnormalities are
also present. The treatment and prognosis of patients with
LVH will depend on the etiology of the LVH. In patients with
hypertension, regression of LVH with antihypertensive
agents is possible. There are clinical data to show that regres-
sion of LVH in patients with hypertension decreases mortal-
ity and morbidity from cardiovascular death.
Right Ventricular Hypertrophy
Right ventricular hypertrophy: Right ventricular
hypertrophy (RVH) is recognized in the ECG by the
following findings (Fig. 7.15).
Abnormalities in the QRS complex
n Right axis deviation of approximately 90. This
should always be present before the diagnosis of
RVH is considered.
n qR complex in V1
n R wave measuring 7 mm in V1
n R wave taller than the S wave in V1 (R/S ratio 1)
n Delayed onset of the intrinsicoid deflection in V1
0.03 seconds
n rS complex from V1 to V6 with right axis deviation
n S1 S2 S3 pattern in adults
Abnormalities in the P wave
n Right atrial abnormality (P-pulmonale)
Chamber Enlargement and Hypertrophy 73
Abnormalities in the ST segment and T wave
n ST segment depression and T wave inversion in
anterior precordial leads (V1 and V2)
In adult patients, the thickness of the right ventricle sel-
dom exceeds that of the left ventricle even when RVH is
present. Because both ventricles are activated simultane-
ously, the forces generated by the right ventricle are
masked by the forces generated by the left ventricle. Thus,
the diagnosis of RVH by ECG may be difficult unless the
right ventricle is severely hypertrophied.
Types of RVH: The ECG manifestations of RVH may
be different. Three different types have been described:
types A, B, and C (Fig. 7.16).
Other Patterns of RVH
Chronic pulmonary disease: When there is chronic
obstructive pulmonary disease such as emphysema or
chronic bronchitis, the overinflated lungs push the di-
aphragm downward, causing the heart to become verti-
cally oriented. When this occurs, the axes of the P wave,
QRS complex, and T wave are all shifted rightward and
inferiorly toward lead aVF (90), resulting in the so
called lead I sign. Because lead I (0) is perpendicular
to lead aVF, lead I and often V6 will conspicuously show
small deflections (Fig. 7.17) because the P, QRS, and T
waves become isoelectric in these leads. The ventricles
also rotate in a clockwise fashion, causing poor R wave
progression and delay in the transition zone. Other
signs of type C RVH like right axis deviation and P-pul-
monale are usually present.
S1 S2 S3 pattern: S1 S2 S3 pattern implies that S waves are
present in leads I, II, and III. When the S1 S2 S3 pattern is
present, the direction of the mean QRS axis is superior
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74 Chapter 7

Figure 7.16:Right Ventricu- A. Type A RVH

lar Hypertrophy. Three types
of right ventricular hypertrophy
(RVH) are shown. (A) Type A RVH.
(B) Type B RVH. (C) An example
of type C RVH.

B. Type B RVH

C. Type C RVH

and to the right, away from leads II and aVF. This
brings the main axis of the QRS complex to the
northwest quadrant, as shown in the ECG in Figure
7.18. S1 S2 S3 pattern is not specific for RVH because it
can occur normally in young children without any
evidence of RVH or cardiac disease. In older individ-
uals, this pattern is suggestive of RVH, especially
when other signs of RVH such as right atrial enlarge-
ment (P-pulmonale) or prominent R waves are pres-
ent in V1. Additionally, the size of the S waves in leads
I, II, and III are usually deeper than the size of the R
waves.
Acute Pulmonary Embolism
Acute pulmonary embolism: Acute pulmonary em-
bolism may also result in acute right heart strain
(Fig. 7.19). Most patients with acute pulmonary em-
bolism are usually ill and restless and are therefore
tachypneic and tachycardic. Sinus tachycardia and in-
complete right bundle branch block are the most fre-
quent ECG findings. The following are the ECG
changes of acute pulmonary embolism.
Rhythm:
n Sinus tachycardia, atrial flutter, or atrial fibrillation
Changes in the QRS complex:
n Right axis deviation of approximately 90
n S1 Q3 T3 pattern (S wave in lead I, Q with in-
verted T wave in III)
n rSR pattern in V1 usually of acute onset
n V1 may also show QS, qR, or R  S pattern
n Clockwise rotation with persistent S in V6 similar
to type C RVH
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Chamber Enlargement and Hypertrophy 75

Figure 7.17: Chronic Obstructive Pulmonary Disease. In chronic obstructive pulmonary disease, the heart
is vertically oriented because of the hyperinflated lungs pushing the diaphragm downward. This causes the P, QRS,
and T deflections to be oriented vertically toward 90 resulting in the so called lead I sign, where all the deflections
in lead I become conspicuous by their diminutive appearance. This could also occur in V6, because V6 is also perpen-
dicular in relation to lead aVF. In addition, the heart is rotated clockwise with peak P-pulmonale in II, III, and aVF.
These changes are consistent with type C RVH.

Changes in the P wave: Combined Ventricular Hypertrophy

n P-pulmonale with peaking of the P waves in
leads II, III, and aVF
n Ta waves become exaggerated in leads II, III, and
aVF, causing 1 mm of ST depression in the infe-
rior leads
Changes in the ST segment and T waves
n ST elevation in V1
n Inverted T waves in V1 to V3 or up to V6
Biventricular hypertrophy: When both the right and
left ventricles are hypertrophied, there is cancellation of
the forces generated by both ventricles. Thus, the ECG
may remain unchanged, and the diagnosis of biventricu-
lar hypertrophy is often difficult. Occasionally, the follow-
ing ECG changes may be present as shown in Fig. 7.20.
Tall biphasic complexes in mid-precordial leads:
The transition leads V3 or V4 may show increased

Figure 7.18: S1 S2 S3 Pattern. This pattern simply implies that an S wave is present in leads I, II, and III.The direc-
tion of the impulse is away from these leads and is usually at the northwest quadrant causing a tall R wave in aVR. S1
S2 S3 may suggest right ventricular hypertrophy in older individuals, especially when the P waves are peaked in lead
II because of right atrial enlargement, when R waves are tall in V1, or the size of the S waves is deeper than the size of
the R waves in all three leads.
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76 Chapter 7

Figure 7.19: Acute Pulmonary Embolism. The electrocardiogram shows sinus tachycardia, right axis devia-
tion 90, S1 Q3 T3 pattern, rR pattern in V1, and persistent S in the precordial leads extending to V6.These findings
are usually acute in onset due to acute right heart strain.

Figure 7.20: Combined Ventricular Hypertrophy. When both ventricles are hypertrophied, the electrocar-
diogram changes of right and left ventricular hypertrophy cancel each other and may be difficult to diagnose. In
this example, there is increased voltage of the QRS complex, especially over the transition zones V3 and V4, which
shows tall R waves and deep S waves. There is also evidence of left ventricular hypertrophy and right atrial enlarge-
ment. Note also that there is voltage discordance, in that the precordial leads show tall voltages, whereas the limb
leads that are bipolar leads have lower voltage.
LWBK271-C07_62-79.qxd 29/1/09 8:55 pm Page 77 LWBK270-4119G-C02_073-110.qxd
amplitude of the QRS complex with increased R
waves combined with deep S waves (Katz-Wachtel
phenomenon).
Right atrial enlargement combined with LVH:
LVH by any standard criteria combined with P pul-
monale as shown in Fig. 7.20.
Voltage discordance: Biventricular hypertrophy
may also manifest as voltage discordance between
the limb and precordial leads. Precordial leads are
unipolar leads and are closer to the heart than the
limb leads. Thus, tall QRS complexes are recorded in
the precordial leads, whereas the limb leads, which
are further away especially bipolar leads I, II, and III,
will record low voltages.
ECG Findings in RVH
Abnormalities in the QRS complexes
Right axis deviation of approximately 90. This should al-
ways be present before the diagnosis of RVH is considered.
qR in V1
R wave in V1 7 mm
Tall R waves in V1 or V2 (R/S ratio 1)
Delayed intrinsicoid deflection in V1 or V2 0.03 seconds.
rS complex from V1 to V6 (clockwise rotation) with right axis
deviation
S1 S2 S3 pattern in adult patients
rSR or RBBB in V1 with right axis deviation
Abnormalities in the P waves
Peaked P waves in leads II, III and aVF (P-pulmonale)
Abnormalities in the ST segment and T waves
ST depression and T wave inversion in right sided precordial
leads (V1)
T wave inversion in V2 to V6
Mechanism
Because of its thinner wall and smaller mass, the right ven-
tricle does not contribute significantly to the generation of
the QRS complex. Thus, when the ventricles are synchro-
nously activated, the forces generated from the right ventri-
cle are masked by those generated from the left ventricle.
When there is RVH, the right ventricular wall becomes
thickened and the right ventricular mass is increased, re-
sulting in a larger contribution of the right ventricle in gen-
erating the QRS complex. In adults, the thickness of the
right ventricle does not exceed that of the left ventricle even
when RVH is present, thus the ECG changes of RVH con-
tinue to be masked by the forces generated by the thicker
Chamber Enlargement and Hypertrophy 77
left ventricle. In certain types of congenital heart diseases,
however, the RV wall is much thicker than the LV wall, such
as in tetralogy of Fallot or in congenital pulmonary steno-
sis. When this occurs, the ECG findings of RVH become
more obvious.
Changes in the frontal or limb leads: RVH is better ap-
preciated in the precordial leads than the limb leads because the
precordial leads overlie the ventricles directly. Nevertheless,
there are certain changes in the limb leads that may suggest
RVH.
Right axis deviation: Right axis deviation is one of the
most reliable signs in the diagnosis of RVH. Because the
right ventricle is anterior and to the right of the left ventri-
cle, increase in right ventricular mass will shift the QRS
axis to the right and anteriorly. Thus, the axis of the QRS
complex is shifted toward 80 to 120 or further to the
right when RVH is present. RVH is the most common
cause of right axis deviation in the adult. The diagnosis of
RVH is unlikely unless the axis of the QRS complex is
shifted to the right.
S1 S2 S3 pattern: This pattern simply means that there
is an S wave in lead I, lead II, and lead III. The presence
of S waves in these leads is due to the terminal forces of
the QRS complex being oriented rightward and superi-
orly toward the northwest quadrant. This is due to acti-
vation of the posterobasal portion of the right ventricle
terminally. The presence of S1 S2 S3, however, is not al-
ways diagnostic of RVH because it is also seen in normal
healthy individuals, especially the younger age group.
When there is S1 S2 S3 pattern, RVH may be present
when other changes in the QRS complex are present,
such as tall R waves in V1, P-pulmonale, or when the S
waves are deeper than the size of the R waves in all three
leads.
Abnormalities of the P wave: Right atrial enlargement
is a frequent accompaniment of right ventricular enlarge-
ment. Thus, the presence of peaked P waves with in-
creased amplitude (P-pulmonale), best recorded in leads
II, III, and aVF suggest RVH unless the P wave changes are
due to tricuspid stenosis, which is rare in adults.
Changes in the precordial leads: Because the precordial
leads are directly on top of the ventricles, more information
is provided by these leads when compared with the more dis-
tal limb leads.
Tall R waves in V1 or V2 with R/S ratio 1: Increased
voltage in the right-sided precordial leads occur when
there is increased thickness of the right ventricular wall.
This will be recorded as tall R waves in V1 or V2 with R/S
ratio 1. R/S ratio 1 means that the height of the R
wave in V1 is equal to or higher in amplitude than the S
wave, which is the reverse of normal in the adult popu-
lation.
rS complex from V1 to V6 with right axis deviation:
This is also called clockwise rotation or delayed transi-
tion. Deep S waves or rS complex from V1 to V6 may be
LWBK271-C07_62-79.qxd 29/1/09 8:55 pm Page 78 LWBK270-4119G-C02_073-110.qxd
78 Chapter 7
due to RVH or LVH. For RVH to be present there should
also be right axis deviation. When RVH is present, the
right ventricle rotates anteriorly, causing the left ventricle
to rotate in a more posterior orientation. If the ventricles
are viewed from below looking upward, the rotation of
both ventricles will be clockwise when there is right ven-
tricular enlargement. Because the precordial leads are
recorded in their standard location from V1 to V6, the tran-
sition zone is not crossed unless the electrodes are moved
to the left and more posteriorly. This type of RVH is fre-
quently associated with chronic lung disease (type C RVH).
Prolonged ventricular activation time with delayed
onset of the intrinsicoid deflection in V1 or V2. When
the ventricular activation time is prolonged, the onset of
the intrinsicoid deflection is delayed. The ventricular acti-
vation time of the right ventricle is measured in V1 from
the onset of the QRS complex to the peak of the R or R
wave and represents the time required for the impulse to
activate the right ventricular wall. The ventricular activa-
tion time of the right ventricle normally measures 0.03
seconds and is increased to 0.04 seconds when there is
right ventricular hypertrophy. The onset of the intrinsi-
coid deflection, measured in V1 or V2, represents the time
when the electrical impulse has reached the right ventric-
ular epicardium and generally coincides with the peak of
the R wave or immediately thereafter, when the R wave is
deflected downward toward baseline.
Clinical Significance
In adults, RVH can result from many different causes. RVH
may be due to pressure overload such as pulmonic stenosis
or primary pulmonary hypertension. This type of RVH pre-
dominantly results in increased thickness of the right ventri-
cle. It may also be due to volume overload such as atrial sep-
tal defect and tricuspid or pulmonic regurgitations,
resulting in volume overload with dilatation of the right
ventricular cavity. RVH can also result from the presence of
lung disease, which may distort the anatomical relationship
between the heart and the chest wall. Or it may be due to left
heart failure where an increase in left ventricular mass is as-
sociated with an increase in right ventricular mass. These
changes may develop insidiously or abruptly, as when pul-
monary hypertension occurs in the setting of acute pul-
monary embolism. The ECG presentations of RVH, there-
fore, in these different clinical settings are not necessarily
similar. Different patterns of RVH have been described
which includes types A, B, and C based on the morphology
of the QRS complex in the precordial leads. Types A and B
are easy to recognize as RVH because the size of the R wave
is taller than the S wave in V1, whereas in type C the size of
the R wave is smaller than the S wave in V1 and may not be
Treatment and Prognosis
recognized as RVH. In all three types, the axis of the QRS
complex is shifted to the right.
Type A RVH: This is the most recognizable type of RVH.
The R waves are tall in V1, often in V2 and V3. The R wave
is usually monophasic (no S wave) in V1. If an S wave is
present, the R wave is always taller than the height of the S
wave with an R/S ratio 1. V5 and V6 may show deeper S
waves than R waves. In type A RVH, the thickness of the
right ventricle is greater than the thickness of the left ven-
tricle, and the right ventricle is the dominant ventricle.
This type of RVH is the most commonly recognized and
is seen in severe pulmonic stenosis, primary pulmonary
hypertension, or mitral stenosis with severe pulmonary
hypertension. The axis of the QRS complex is signifi-
cantly deviated to the right at approximately 120.
Type B RVH: The R wave in V1 is slightly taller than the S
wave or the ratio between the R wave and S wave is 1. V1
may also exhibit an rsr pattern. The QRS complex in V5
and V6 is not different from normal. This type of RVH is
usually due to atrial septal defect or mitral stenosis with
mild to moderate pulmonary hypertension. The frontal
axis is vertical at approximately 90.
Type C RVH: This type of RVH is difficult to recognize
and is frequently missed because the R wave in V1 is not
tall and is smaller than the S wave. Instead, a deep S wave
is present in V1 and in V2 that extends up to V6. Thus, V1
to V6 will show rS complexes. In V6, the R wave continues
to be smaller in amplitude than the S wave. The axis of the
QRS complex is approximately 90 or less. This type of
RVH is usually due to chronic obstructive lung disease
but could also occur acutely as a manifestation of acute
pulmonary embolism.
Prolongation of the QRS complex usually does not occur
when there is RVH because the thickness of the right ventri-
cle wall usually does not exceed that of the left ventricle, even
when RVH is present. Thus, the forces generated by the right
ventricle are cancelled by the forces from the left ventricle.
When widening of the QRS complex is present, there may be
associated right bundle branch block because the right bun-
dle branch is very susceptible to injury when there is in-
creased right ventricular pressure.
The right ventricle is to the right and anterior to that of the
left ventricle. Pulsations from the right ventricle are not nor-
mally visible or palpable. However, when the right ventricle
is enlarged or hypertrophied, a sustained systolic precordial
impulse is palpable along the left parasternal area. Prominent
a waves are seen in the neck veins. Very often, tricuspid re-
gurgitation is also present causing a cv wave in the jugular
neck veins accompanied by prominent pulsations of the liver
or the ear lobes bilaterally. Third and fourth gallop sounds
may also be audible along the lower left sternal border. Their
right ventricular origin can be verified by increase in inten-
sity of these gallop sounds with inspiration.
When RVH is present, the underlying cause should be evalu-
ated. The treatment and prognosis will depend on the etiol-
ogy of the RVH.
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8
Atrioventricular Block
Types of AV Block
The atria and ventricles are contiguous structures sep-
arated by a dense mass of fibrous tissues that are elec-
trically inert. This prevents the direct spread of electri-
cal impulses between the atria and ventricles. The only
pathway by which the sinus impulse can reach the ven-
tricles is through the normal atrioventricular (AV)
conduction system (Fig. 8.1).
The normal AV conduction system consists of the AV
node, bundle of His, bundle branches, and fascicular
branches of the left bundle branch. The sinus impulse
can be delayed or interrupted anywhere along this con-
duction pathway, resulting in varying degrees of AV
block.
There are three types of AV block based on the severity
of the conduction abnormality:
First-degree AV block
Second-degree AV block
n Mobitz type I or AV Wenckebach
n Mobitz type II
n Advanced or high grade
Third-degree or complete AV block
Figure 8.1:Diagrammatic Repre- Sinus
sentation of the Atrioventricular Node
(AV) Conduction System. The atria
and ventricles are separated by a dense
mass of fibrous tissues. This prevents Dense
the spread of atrial impulses directly to Fibrous
the ventricles. The only pathway by Tissues
which the atrial impulse can propagate
to the ventricles is through the AV
conduction system.
Ventricles
80
First-Degree AV Block
Normal AV conduction: The normal PR interval
measures 0.12 to 0.20 seconds in the adult (Fig. 8.2). It
represents the time required for the sinus impulse to
travel from atria to ventricles.
First-degree AV block: First-degree AV block simply
means that the PR interval is prolonged and measures
0.20 seconds (Fig. 8.3). It indicates delay in the con-
duction of the sinus impulse from atria to ventricles
with most of the delay occurring at the level of the AV
node.
Although the PR interval is prolonged in first-degree
AV block, all P waves are conducted to the ventricles
and are always followed by QRS complexes (Fig. 8.4).
First-degree AV block therefore is a conduction delay
rather than actual block. This conduction delay can oc-
cur anywhere between the atria and the ventricles.
First-degree AV block is usually a conduction delay at
the AV node. This can be due to a variety of causes in-
cluding enhanced vagal tone; use of pharmacologic
agents that prolong AV conduction such as beta
blockers, calcium channel blockers, and digitalis; or it
might indicate disease of the AV conduction system.
Atria
AV Node
AV
Conduction
Bundle of His
System
Bundle Branches
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Atrioventricular Block 81

QRS 0.20 second

PR Interval = 0.15 second

P T

Figure 8.2: Normal Atrioventricular (AV) Conduction. Rhythm strip showing

normal PR interval measuring 0.15 seconds. The PR interval is measured from the beginning
of the P wave to the beginning of the QRS complex and normally varies from 0.12 to 0.20 sec-
onds. If a Q wave is present, the PR interval is measured from the beginning of the P wave to
the beginning of the Q wave (P-Q interval). The PR interval represents the time required for
the sinus impulse to travel from atria to ventricles.

Once a sinus P wave is not conducted to the ventri-

cles, the AV block has advanced to second degree
(Fig. 8.5).
Common Mistakes in First-Degree
AV Block
The diagnosis of first-degree AV block is usually
straightforward but can be very confusing if the PR in-
terval is unusually prolonged. The P wave may be hid-
den within the T wave or it can be mistaken for a
T wave of the previous complex (Figs. 8.6C and 8.7).
First-degree AV block does not cause symptoms. How-
ever, when the P wave falls within the Q-T interval of
the previous cardiac cycle, which corresponds to ven-
tricular systole, simultaneous contraction of both atria
and ventricles may cause symptoms of low cardiac out-
put (Figs. 8.6C and 8.7).
First-Degree AV Block
Electrocardiogram Findings
1. The PR interval is prolonged and measures 0.20 seconds.
2. Every P wave is followed by a QRS complex.
Mechanism
The PR interval represents the time required for the sinus
impulse to travel from atria to ventricles. There are several
structures involved in the propagation of the sinus impulse
to the ventricles. These include the atria, AV node, His bun-
dle, bundle branches, and fascicles. The sinus impulse can be
delayed anywhere between the atria and ventricles although
the prolongation of the PR interval is almost always due to
slowing of conduction within the AV node. Less commonly,
first-degree AV block can occur in the His-Purkinje system or
within the atria.

0.20 second
Figure 8.3: First-Degree
Atrioventricular (AV) Block.
Rhythm strip showing PR interval of
PR interval = 0.34 second
QRS 0.34 seconds. Any PR interval meas-
uring 0.20 seconds is first-degree
T AV block and indicates that there is a
P
delay in the conduction of the sinus
impulse from atria to ventricles.
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82 Chapter 8

0.20 second
PR Interval = 0.42 second

Figure 8.4: First-Degree Atrioventricular (AV) Block. The PR interval measures

0.42 seconds and is unusually prolonged. Regardless of the duration of the PR interval as
long as every P wave is followed by a QRS complex, the conduction abnormality is first-
degree AV block.

Figure 8.5: Second-Degree Atrioventricular (AV) Block. When a sinus P wave is not
conducted to the ventricles and is not followed by a QRS complex (star), the conduction
abnormality is no longer first-degree but has advanced to second-degree AV block.

Lead II Rhythm Strips

A PR = 0.20 second

B PR = 0.36 second

C PR = 0.41 second

Figure 8.6: First-Degree Atrioventricular (AV) Block. When the PR interval is un-
usually prolonged, the P wave may be mistaken for a T wave. Rhythm strips (A, B, C) are
from the same patient taken on separate occasions. (A) Top normal PR interval of 0.20 sec-
onds. Arrows identify the P waves.The PR interval is longer in (B) (0.36 seconds) and is
even much longer in (C) (0.41 seconds). In (C), the PR interval is unusually prolonged such
that the P waves can be mistaken for T waves of the previous complex.

PR Interval = 0.46 second

P P P

Figure 8.7: First-Degree Atrioventricular (AV) Block with Unusually Prolonged

PR Interval. The PR interval measures 0.46 seconds and is unusually prolonged.The P wave
is difficult to recognize (arrows) because it is superimposed on the T wave of the previous
complex.This can result in synchronous contraction of both atria and ventricles, which may
cause symptoms of low cardiac output.
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Clinical Significance
First-degree AV block is the mildest form of AV conduction
abnormality characterized by delay in conduction of the si-
nus impulse from atria to ventricles. All P waves conduct to
the ventricles, thus first-degree AV block is a misnomer be-
cause the impulse is only delayed. There is no actual block.
First-degree AV block may not be appreciated if the PR inter-
val is markedly prolonged or the P wave is buried within the
T wave of the previous complex. In both instances, the P
wave may be difficult to identify.
First-degree AV block can be the result of enhanced vagal
tone; administration of pharmacologic agents that can block
the AV node such as beta blockers, calcium blockers, digitalis;
and other antiarrhythmic agents. It can be caused by hy-
pothyroidism, rheumatic fever, or intrinsic disease of the AV
node and conducting system from ischemia, inflammation,
infiltration, and fibrosis.
The first heart sound is usually diminished in intensity
when there is first-degree AV block. If the PR interval is pro-
longed, the AV valves slowly drift back to a semiclosed posi-
tion before the ventricles contract, resulting in a soft first
heart sound. When the PR interval is unusually prolonged
and the P wave is inscribed at the T wave or ST segment of
the preceding complex, cannon A waves may be seen in the
jugular neck veins because atrial contraction occurs simul-
taneously with ventricular systole, which may result in di-
minished cardiac output.
Treatment
First-degree AV block is benign and does not require any
treatment. The etiology of the AV block should be recognized
and corrected.
First-degree AV block may compromise left ventricular fill-
ing if the PR interval is 0.30 seconds because atrial con-
traction may occur during ventricular systole. This may ele-
vate atrial and pulmonary venous pressures and reduce
ventricular filling and cardiac output resulting in symptoms
of congestion and low output very similar to the symptoms
associated with the pacemaker syndrome (see Chapter 26,
The ECG of Cardiac Pacemakers). If the long PR interval is
not reversible and temporary AV pacing can improve the
symptoms related to low cardiac output, the American Col-
lege of Cardiology (ACC), American Heart Association
Figure 8.8: Type I Second-Degree Atrioventricular (AV) Block. The rhythm strip
shows type I second-degree AV block.Three P waves are conducted with gradual prolongation
of the PR interval. Only one P wave (marked by the arrows) is not followed by a QRS complex.
Atrioventricular Block 83
(AHA), and Heart Rhythm Society (HRS) guidelines for
permanent pacemaker implantation consider this type of
first-degree AV block as a class IIa indication for permanent
pacing (meaning that the weight of evidence is in favor of
usefulness or efficacy of the procedure).
Prognosis
Prognosis is generally good and favorable especially if the
cause is reversible. If the cause is due to structural cardiac ab-
normalities, first-degree AV block may progress to higher
grades of AV block. The prognosis therefore depends on the
associated cardiac abnormalities rather than the presence of
first-degree AV block.
Second-Degree AV Block
Second-degree AV block: There are three types of
second-degree AV block.
Mobitz type I also called AV Wenckebach
Mobitz type II
Advanced, also called high-grade second-degree AV
block
Type I and type II second-degree AV block: In type
I and type II second-degree AV block, two or more con-
secutive P waves are conducted to the ventricles and
only single P waves are blocked (Fig. 8.8).
Advanced second-degree AV block: The AV block is
advanced when the second-degree block cannot be clas-
sified as type I or type II. An example of advanced sec-
ond-degree AV block is when two or more consecutive
P waves are blocked as in 3:1, 4:1, or 5:1 AV block (Fig.
8.9). Another example is when only a single P wave is fol-
lowed by a QRS complex as in 2:1 AV block (Fig. 8.10).
Type I Second-Degree AV Block
Type I second-degree AV block: Type I second-de-
gree AV block is also called AV Wenckebach. The fol-
lowing features characterize type I second-degree AV
block (Figs. 8.11 and 8.12):
Two or more consecutive P waves are conducted.
Only single P waves are blocked.
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84 Chapter 8

Figure 8.9: Advanced 3:1 Second-Degree Atrioventricular (AV) Block. The

rhythm strip shows intermittent 3:1 AV block (brackets). The first two P waves are not
conducted. When two or more consecutive P waves are not conducted, the rhythm is
advanced second-degree block. Arrows point to the P waves.

Figure 8.10: Advanced 2:1 Second-Degree Atrioventricular (AV) Block. In 2:1 AV

block, the first P wave is conducted and the next P wave is blocked (arrows). A common error is
to classify 2:1 AV block as a type II second-degree AV block. Because only one P wave is followed
by a QRS complex, the AV block cannot be classified as type I or II.

PR = 0.18 sec 0.27 sec 0.33 sec PR = 0.18 sec

Pause

#1 #2 #3 #4 #5

Figure 8.11: Type I Second-Degree Atrioventricular (AV) Block. The rhythm strip
shows 4:3 AV Wenckebach with four P waves (labeled 1 to 4) conducting only three QRS com-
plexes. The PR interval gradually prolongs before a ventricular complex is dropped (star). The
long pause allows the conduction system to rest and recover so that the next P wave (5) is
conducted more efficiently, resulting in a PR interval that measures the shortest. The QRS
complexes are narrow and only a single P wave is not conducted (4).

PR interval is longest PR interval is shortest

before the pause after the pause

Pause
Pause

#1 #2

Figure 8.12: Type I Second-Degree Atrioventricular (AV) Block. Instead of measur-

ing for gradual prolongation of the PR interval, one can simply compare the PR interval before
(1) and after (2) the pause. If the PR interval shortens after the pause, type I AV block is present.
The stars identify single P waves that are not conducted.
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Atrioventricular Block 85

#1 #2 #3 #4

Figure 8.13: Group Beating. Group beating simply means that if you eyeball the trac-
ing from left to right, one gets the impression that the beats (the QRS complexes) are
grouped together because of the spaces created by P waves without QRS complexes (stars).
Four such groups can be identified in the above tracing (groups 1 to 4). Group beating is fre-
quently seen in type I atrioventricular (AV) block because AV Wenckebach has a tendency to
be repetitive. The above is an example of 4:3 AV Wenckebach meaning that there are four P
waves for every three QRS complexes.

There is gradual prolongation of the PR interval be-
fore a ventricular complex is dropped.
The PR interval always shortens immediately after
the pause.
The QRS complexes may be narrow or wide but are
typically narrow.
Type I Second-Degree AV Block
There are additional features commonly seen in classi-
cal type I second-degree AV block:
Group beating is present (Fig. 8.13)
The R-R intervals (distance between two R waves)
are variable (Fig. 8.14). The R-R interval straddling
a blocked P wave is less than the R-R interval strad-
dling a conducted sinus impulse.
Conduction ratio: The conduction ratio refers to the
total number of P waves to the total number of QRS
complexes that are conducted. Thus, a 4:3 AV
Wenckebach implies that of four consecutive P waves,
only three are conducted; a 5:4 AV Wenckebach
means that of five consecutive P waves, only four are
conducted.
Shortening of the PR interval after a pause is much eas-
ier to recognize than gradual prolongation of the PR
interval, as shown in Figure 8.15. This always favors
second-degree type I AV block.
Type I second-degree AV block may have narrow or
wide QRS complexes.
Localizing the AV block: Type I second-degree AV
block is almost always localized at the level of the AV
node, although it can also occur below the AV node
(infranodal) at the level of the His-Purkinje system.
The presence of bundle branch block (Fig. 8.16) or my-
ocardial infarction (Fig. 8.17) may be helpful in localiz-
ing whether the block is nodal or infranodal.
Narrow QRS complexes: When the QRS com-
plexes are narrow, the block is almost always con-
fined to the AV node (Fig. 8.18). A block occurring
at the bundle of His (intra-His block) is possible,
but is rare.
Wide QRS complexes: When the QRS complexes
are wide because of the presence of bundle branch
block, the block may be AV nodal although an infra-
nodal block at the level of the bundle branches is
more likely (Fig. 8.16).

1.52 s

1.2 s 0.80 s 0.72 s

Pause

Figure 8.14: Varying R-R Interval in Type I Second-Degree Atrioventricular

(AV) Block. Type I can be differentiated from type II second-degree AV block by the R-R
intervals. In type I AV block, the R-R intervals are variable because the PR intervals are also
variable. Note that the R-R interval straddling a blocked P wave (1.2 seconds) is less than the
R-R interval straddling a conducted sinus impulse (1.52 seconds). This is in contrast to type
II block, where the R-R intervals are fixed because the PR intervals are also fixed (see Fig.
8.20).The longest R-R interval occurs immediately after the pause (0.80 seconds) with grad-
ual shortening of the next R-R interval (0.72 seconds). The stars mark the P waves that are
not conducted.
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86 Chapter 8

PR interval
PR interval shortens after
longer the pause

Pause

Figure 8.15: Type I Second-Degree Atrioventricular (AV) Block. The PR interval looks
fixed but suddenly shortens after the pause.The shortening of the PR interval is characteristic of
type I second-degree AV block. The star identifies a P wave without a QRS complex. Note that
gradual lengthening of the PR interval is not obvious before the pause.

Acute myocardial infarction (MI):
n Acute inferior MI: When AV block occurs in the
setting of an acute inferior MI, the location of the
AV block is at the AV node (Fig. 8.17, see also Figs.
8.30 and 8.39). The QRS complexes are narrow.
n Acute anterior MI: When AV block occurs in the
setting of an acute anterior MI, the AV block
is below the AV node (infranodal block). The
QRS complexes are usually wide (See section on
Complete AV Block).
3. There is gradual prolongation of the PR interval before a ven-
tricular complex is dropped.
4. The PR interval always shortens immediately after the
pause.
5. The QRS complexes are usually narrow.
6. Group beating is present.
7. The R-R intervals are variable. The longest R-R interval is
noted immediately after the pause and shortening of the R-R
interval occurs successively thereafter.

ECG Findings of Type I AV Block Mechanism

1. Two or more consecutive P waves are conducted. Type I second-degree AV block or AV Wenckebach is usu-
2. Only single P waves are blocked. ally a block at the level of the AV node although it can occur

PR = 0.32 sec PR = 0.25 sec

Figure 8.16: Second-Degree Atrioventricular (AV) Block with Wide QRS Complexes. The QRS
complexes in AV Wenckebach are usually narrow. In this example, the QRS complexes are wide because of the pres-
ence of right bundle branch block and left anterior fascicular block. The rhythm strip at the bottom of the tracing
shows 3:2 AV Wenckebach. Note that the PR interval is longer before the pause (0.32 seconds) and shortens immedi-
ately after the pause (0.25 seconds). Shortening of the PR interval after the pause is consistent with type I second-
degree AV block. The P waves that are not conducted are identified by the stars.
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Atrioventricular Block 87

Figure 8.17: Atrioventricular (AV) Block and Acute Inferior Myocardial Infarction (MI). When type I
block occurs in the setting of acute inferior MI as shown, the block is AV nodal. The stars identify the blocked P waves.

anywhere in the AV conduction system. When the QRS com-
plexes are narrow, the block is almost always AV nodal. A
block in the distal His-Purkinje system is suspected when
there is bundle branch block (a sign of distal conduction sys-
tem disease) or when the AV block occurs in the setting of an
acute anterior MI.
Because the sinus impulses constantly bombard the AV
node, conduction through the AV node becomes progres-
sively delayed until a sinus impulse can no longer be con-
ducted, resulting in a P wave without a QRS complex. The
pause allows the AV node to rest and recover, allowing the
next impulse to be conducted more efficiently resulting in a
shorter PR interval.
Clinical Significance
Type I AV block may be a normal finding in healthy individ-
uals, especially during sleep, because of enhanced vagal tone.
It may be caused by intense vagal stimulation such as vomit-
ing or coughing. The arrhythmia may be caused by agents
that block the AV node, such as calcium blockers, beta block-
ers, or digitalis. These examples of AV block are the result of
extrinsic causes and are reversible. AV block can also be due
to structural cardiac disease such as degenerative and calcific
disease of the conduction system, ischemia, infarction or in-
flammation of the AV node, or intraventricular conduction
system including acute myocarditis, rheumatic fever, and
Lyme disease. These examples of AV block are due to intrin-
sic disease of the AV node and conduction system and may
not be reversible.
Type I AV block is usually confined to the AV node. The QRS
complexes are narrow. Type I AV block with wide QRS com-
plexes may be AV nodal but is more frequently infranodal.
When the block is infranodal, the cause of the AV block is
usually due to structural cardiac disease.
AV nodal block: AV block at the level of the AV node is
generally benign with a good prognosis. Even when type I
block progresses to complete AV block, the AV block is
usually reversible. Furthermore, the rhythm that comes to
the rescue (escape rhythm), is from the AV junction.

3:2 AV
Wenckebac 2:1 AV Block

Figure 8.18: Two to One Atrioventricular (AV) Block. The initial portion of the trac-
ing shows a classical 3:2 AV Wenckebach with gradual prolongation of the PR interval. This is
followed by 2:1 AV block. The presence of 2:1 block associated with classical AV Wenckebach
with narrow QRS complexes suggests that the 2:1 AV block is AV nodal. The stars identify the
P waves.
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88 Chapter 8

AV Nodal Block Infranodal Block

A B C D

A.

B.

Figure 8.19: Complete Atrioventricular (AV) block and Junctional Escape Rhythm. Complete AV
block can occur anywhere in the conduction system. In the upper column, complete AV block is at the AV node
(A); in (B), at the bundle of His; in (C), both bundle branches; and in (D), right bundle branch and both fascicles of
the left bundle. If the block is AV nodal (A), the escape rhythm will be AV junctional (star) and will have narrow QRS
complexes (electrocardiogram A). However, if the block is infranodal (diagrams B, C, and D), AV junctional rhythm
is not possible and the escape rhythm will be ventricular with wide QRS complex (electrocardiogram B).

AV junctional rhythm is more stable and more physio-
logic than a ventricular escape rhythm and has a relatively
fast rate that can be further enhanced with atropine.
Infranodal block: Type I block with wide QRS com-
plexes may be nodal or infranodal. Infranodal AV block
may occur at the level of the bundle of His, bundle
branches, or distal fascicles. Infranodal AV block is almost
always associated with bundle branch block and the im-
mediate prognosis is more ominous when compared with
that occurring at the AV node (Fig. 8.19).
Type I AV block is a common complication of acute infe-
rior MI and is usually reversible since the block is at the
level of the AV node.
Treatment
Symptomatic patients:
For symptomatic patients with type I second-degree AV
block that does not resolve, especially in patients with left
ventricular systolic dysfunction, the ACC/AHA/HRS
guidelines recommend the insertion of a permanent
pacemaker as a Class I indication regardless of the loca-
tion of the AV block. (Class I means there is evidence or
general agreement that the procedure is beneficial, useful,
and effective.)
Patients with second-degree AV block with symptoms
similar to those of the pacemaker syndrome; insertion of
a permanent pacemaker is a Class IIa recommendation.
Patients with neuromuscular disease with second-degree
AV block with or without symptoms; insertion of a per-
manent pacemaker is a Class IIb recommendation.
Asymptomatic patients: Type I second-degree AV nodal
block is usually reversible and generally does not require any
therapy. The cause of the AV block should be identified and
corrected. The following are the ACC/AHA/HRS recommen-
dations regarding insertion of permanent pacemakers in
completely asymptomatic patients with type I second-degree
AV block.
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AV nodal block:
n If the block is AV nodal and the patient is hemody-
namically stable and asymptomatic, with a heart rate
50 beats per minute (bpm), insertion of a permanent
pacemaker is a Class III recommendation. Class III
means that there is evidence or general agreement that
the procedure is not useful and in some cases may be
harmful.
n If the block is AV nodal and is expected to resolve and
unlikely to recur (such as effect of drugs, Lyme dis-
ease, hypoxia from sleep apnea), permanent pacing is
also a Class III recommendation.
Infranodal block:
n If the AV block is infranodal, at the level of the bundle
of His (intra-His) or bundle branches (infra-His), in-
sertion of a permanent pacemaker is a Class IIa indi-
cation. This includes asymptomatic patients with
infranodal block diagnosed during an electrophysio-
logic study for other indications.
Any level: Some patients with second-degree AV block at
any level may be completely asymptomatic, but may need
permanent pacing for the following conditions:
n Patients who develop second of third-degree AV block
during exercise in the absence of myocardial ischemia.
This is a Class I recommendation.
n Myotonic muscular dystrophy, Erb dystrophy, and
peroneal muscular dystrophy with any degree of AV
block (including first-degree AV block) with or with-
out symptoms because of unpredictable progression
of AV conduction disease. This is a class IIb recom-
mendation.
Emergency treatment of symptomatic patients with
bradycardia includes atropine (see Treatment of Com-
plete AV Block in this Chapter) and if not effective, a
temporary transvenous or transcutaneous pacemaker
may be necessary before a permanent pacemaker can be
implanted.
Other pharmacologic agents that can be tried for treat-
ment of the bradycardia before a pacemaker can be in-
serted include adrenergic agents such as isoproterenol,
epinephrine, or dobutamine. These are further dis-
PR interval = 0.20 second throughout
Figure 8.20: Type II Second-Degree Atrioventricular (AV) Block. In Mobitz type II
AV block, the PR intervals are fixed and measure the same throughout. It does not lengthen
before nor shorten after a QRS complex is dropped. Note that only single P waves are
blocked (stars) and that the QRS complexes are wide because of the presence of a bundle
branch block.
Atrioventricular Block 89
cussed under treatment of complete heart block in this
chapter.
Prognosis
Type I AV block most often occurs at the level of the AV node
and is usually reversible with a good prognosis. The AV block
is often seen in normal healthy athletic individuals, especially
during sleep.
If the AV block occurs more distally at the level of the His-
Purkinje system, structural cardiac disease is usually pres-
ent. The overall prognosis in these patients will depend on
the underlying cardiac abnormality. If the underlying
cause is degenerative disease confined to the conduction
system, the prognosis is similar to a patient without the
conduction abnormality after a permanent pacemaker is
implanted.
Type II Second-Degree AV Block
Mobitz type II second-degree AV block: Mobitz
type II second-degree AV block is characterized by the
following features:
Two or more consecutive P waves are conducted.
Only single P waves are blocked.
All PR intervals measure the same throughout. The
PR interval is fixed and does not prolong before or
shorten after a pause (Figs. 8.20 and 8.21).
The QRS complexes are usually wide (Figs. 8.20 and
8.21) because of the presence of bundle branch
block.
The R-R intervals (distance between R waves) are
constant and measure the same throughout as long
as the sinus rhythm is stablethat is, the heart rate
or P-P intervals are regular (Fig. 8.22).
Type II block with wide QRS complexes: Mobitz
type II second-degree AV block is always an infran-
odal block and occurs exclusively at the level of the
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90 Chapter 8

PR interval = 0.20 second throughout

Figure 8.21: Type II Second-Degree Atrioventricular (AV) Block. The PR intervals

are fixed (distances between paired arrows measure 0.20 seconds throughout). The QRS
complexes are wide and only single P waves are not conducted (stars).

His-Purkinje system (Fig. 8.23). Type II block is un-
likely unless there is evidence of infranodal disease
such as bundle branch block or anterior MI.
Type II block with narrow QRS complexes: Type II
block with narrow QRS complexes is possible, al-
though rare. The block involves the His bundle (intra-
His block) rather than the bundle branches. If the PR
interval looks fixed, but the QRS complexes are narrow
and no evidence of anterior MI is present, the block
may be AV nodal rather than infranodal. More often,
the PR interval looks fixed because there is only mini-
mal prolongation in the surface electrocardiogram
(ECG), which is difficult to demonstrate unless the PR
interval is measured carefully (Fig. 8.24).
Treatment: Even in completely asymptomatic pa-
tients, a permanent pacemaker should be considered
when the diagnosis is type II second-degree AV block.
Type II AV block with wide QRS complexes: In-
sertion of a permanent pacemaker is a Class I indi-
cation for patients with type II second-degree AV
block associated with wide QRS complexes.
Type II AV block with narrow QRS complexes: If
the QRS complexes are narrow and type II second-
degree AV block is present, insertion of a permanent
pacemaker is a Class IIa indication. If the level of the
AV block is uncertain, an electrophysiologic study
should be performed before a permanent pace-
maker is implanted.
Prognosis: Because type II second-degree AV block is
an infranodal disease, the immediate prognosis is more
ominous than type I AV block, where the block is usu-
ally AV nodal (Fig. 8.25). Infranodal disease is associ-
ated with structural heart disease and is progressive
and usually not reversible. When complete AV block
occurs, it is usually sudden without warning.
ECG Findings of Type II Second-degree AV Block
1. Two or more consecutive P waves are conducted.
2. Only single P waves are blocked.
3. The PR intervals are fixed and do not vary. The PR interval
does not prolong before or shorten after the pause.
4. The QRS complexes are wide due to the presence of bundle
branch block.
5. If the sinus rate is stable, the R-R intervals are fixed. The R-R
interval between three successively conducted sinus complexes
is equal to the R-R interval straddling the pause.
Mechanism
In Mobitz type II second-degree AV block, one bundle
branch has a fixed block and the other bundle branch is in-
termittently blocked, resulting in P waves that are not con-
ducted. The PR interval remains constant throughout. The
PR interval immediately after the pause should not shorten
and should measure the same as the PR interval before the
pause.
Mobitz type II second-degree AV block occurs exclusively at
the His-Purkinje system, usually at the level of the bundle
branches. Although the block can occur within the His bun-
dle, an intra-His block is rare. Before the diagnosis of type II
block is secured, there should be evidence of infranodal dis-
ease in the form of left bundle branch block or right bundle

B
A C

Figure 8.22: Constant R-R Intervals. In type II second-degree atrioventricular (AV)

block, the R-R intervals are constant because the PR intervals are also constant. Distance A
and C with three consecutive complexes measure the same as distance B with a dropped
QRS complex. Thus, the RR interval straddling a pause (distance B) measures the same as
the R-R interval straddling a conducted sinus impulse (A or C). The P waves are marked by
the arrows.
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Atrioventricular Block 91

Figure 8.23: Mobitz Type II Second-Degree Atrioventricular (AV) Block. The 12-lead electro-
cardiogram shows all the findings of type II second-degree AV block. The PR interval is fixed, only single P
waves are blocked (stars), two consecutive P waves are conducted, and there is left bundle branch block.

Figure 8.24: Fixed PR Interval with Narrow QRS Complexes. The PR interval looks fixed and the
QRS complexes are narrow. However, if the PR interval is measured carefully, there is subtle shortening imme-
diately after the pause. Shortening of the PR interval after a pause suggests type I second-degree atrioventric-
ular block. The stars identify the nonconducted P waves.

Atria Atria

AV Node

His Bundle

Bundle Branches

Ventricles Ventricles

A: Type I B: Type II
Figure 8.25: Location of Atrioventricular (AV) Block. In type I second-degree AV block or AV
Wenckebach (A), the AV block is almost always at the AV node although it can also occur anywhere in the
His-Purkinje system. In type II second-degree AV block (B), the AV block occurs exclusively at the bundle of
His, bundle branches, and distal conduction system. The lines transecting the AV conduction system indi-
cate the potential sites of AV block.
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92 Chapter 8
branch block with or without fascicular block. When one
bundle branch is blocked, intermittent block of the other
bundle causes the QRS complex to be dropped intermit-
tently. If the QRS complex is narrow and the PR interval
looks fixed, the possibility of a block at the level of the bun-
dle of His is likely (intra-His block), although this is rare and,
more commonly, may be due to AV nodal block with mini-
mal prolongation of the PR interval that may be difficult to
appreciate in the surface ECG unless the PR interval is meas-
ured carefully.
Clinical Significance
Type II block is an infranodal disease involving the bundle of
His, and, more commonly, the bundle branches and fascicles.
Type II block does not occur at the level of the AV node.
It is a common mistake to include 2:1 AV block as Mobitz
type II block. It is not possible to distinguish type I from type
II block when there is 2:1 AV block because prolongation of
the PR interval cannot be observed when only one P wave is
conducted. In 2:1 AV block, the PR interval looks fixed be-
cause only a single P wave is conducted.
When an acute infarct is complicated by type II second-de-
gree AV block, the location of the infarct is anterior. Even
with insertion of a pacemaker, mortality remains high be-
cause an anterior infarct with second-degree AV block is usu-
ally an extensive infarct.
If there is difficulty in differentiating type I (usually AV nodal)
from type II (always infranodal) block, sympathetic and
parasympathetic manipulation may be tried. Both sinus node
and AV node are influenced by sympathetic and parasympa-
thetic stimulation, whereas the intraventricular conduction
system below the AV node is affected mainly by sympathetic
but not by parasympathetic stimuli. Sympathetic stimulation
such as exercise increases the rate of the sinus node and en-
hances conduction across the AV node. Atropine and adrener-
gic agents can cause the same effect. Thus, exercise, atropine,
or adrenergic agents will increase the sinus rate and will also
improve AV nodal block, but will not improve and may even
worsen type II or infranodal block. On the other hand,
parasympathetic stimulation such as carotid sinus compres-
sion can improve infranodal block by slowing the sinus rate
and prolonging AV conduction, thus allowing the distal con-
duction system and infranodal block more time to recover.
Type II block is usually caused by structural cardiac disease
such as sclerosis or calcification of the conducting system re-
sulting from aging. It can also be due to ischemia, infarction,
and infiltrative diseases including sarcoid, amyloid, and neu-
romuscular dystrophy. It can occur postoperatively after car-
diac surgery or ablation procedures.
Treatment
Because type II block is an infranodal disease, a permanent
pacemaker should be inserted even in asymptomatic pa-
tients. If type II AV block is associated with wide QRS com-
plexes, this is a Class I indication for permanent pacing, ac-
cording to the ACC/AHA/HRS guidelines. If the QRS com-
plexes are narrow, the recommendation becomes Class IIa.
Patients with type II block can develop complete heart block
suddenly without warning. Thus, a transcutaneous pace-
maker or a temporary pacemaker should be available even if
the patient is not bradycardic. If the patient suddenly devel-
ops complete AV block before a pacemaker can be inserted,
adrenergic agents such as isoproterenol or epinephrine may
be given to increase the intrinsic rate of the escape rhythm.
Infranodal block will not respond to atropine (see Treatment
of Complete AV Block in this Chapter).
When the QRS complexes are narrow and the PR intervals
look fixed, the diagnosis of Mobitz type II block may be
questionable. If the diagnosis of type II block is uncertain, an
electrophysiologic study may be necessary to ascertain that
the block is infranodal before a permanent pacemaker is im-
planted, especially in asymptomatic patients with second-
degree AV block.
Prognosis
Because type II block is an infranodal disease, the immedi-
ate prognosis is more ominous than type I second-degree
AV block. When complete AV block occurs, the escape
rhythm has to originate below the level of the block. Thus,
only a ventricular escape rhythm can come to the rescue.
Unlike type I block, type II block is commonly associated
with structural heart disease; therefore, the conduction
abnormality is usually not reversible and progression to
complete AV block may be sudden without warning (see
complete AV block).
The overall prognosis of type II block depends on the pres-
ence or absence of associated cardiac abnormalities.
If the AV block is confined to the conduction system and
no evidence of structural cardiac disease is present, inser-
tion of a permanent pacemaker to correct the conduction
abnormality will result in the same natural history as a
patient without the conduction abnormality.
If the conduction abnormality is associated with struc-
tural cardiac disease, such as ischemic heart disease or
cardiomyopathy, the prognosis will depend on the etiol-
ogy of the cardiac abnormality.
Advanced 2:1 Second-Degree AV Block
Advanced second-degree AV block: 2:1 AV block is
an example of advanced second-degree AV block.
In 2:1 block, every other P wave is conducted alter-
nating with every other P wave that is blocked
(Figs. 8.26 and 8.27).
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Atrioventricular Block 93

870 ms 820 ms 870 ms 820 ms

Figure 8.26: 2:1 Second-Degree Atrioventricular (AV) Block with Narrow QRS Complexes. Every
other P wave is conducted alternating with every other P wave that is blocked (arrows) consistent with 2:1 AV
block. Two to one AV block is not a type II block because only a single P wave is conducted. Note that the QRS com-
plexes are narrow, thus an infranodal block is unlikely. Because there is no evidence of distal conduction system
disease, the 2:1 AV block is most likely at the level of the AV node. Note also that the P-P interval with a QRS
complex is shorter (820 milliseconds) than the P-P interval without a QRS complex (870 milliseconds) because of
ventriculophasic sinus arrhythmia.

The QRS complexes may be narrow or wide (Figs.
8.26 and 8.27).
A common error is to include 2:1 AV block as a type
II block because the PR interval is fixed. Two to one
AV block is neither type I nor type II second-degree
block. The PR interval looks fixed because only a
single P wave is conducted, thus only one PR inter-
val can be measured. To differentiate type I from
type II block, at least two consecutive P waves
should be conducted so that the lengthening of the
PR interval can be observed.
Ventriculophasic sinus arrhythmia: During 2:1 AV
block, sinus arrhythmia may be present. The sinus ar-
rhythmia is ventriculophasic if the P-P interval with a
QRS complex is shorter than the P-P interval without a
QRS complex (Fig. 8.26).
2:1 AV block may be nodal or infranodal. To differenti-
ate one from the other, continuous monitoring should
be performed until conduction improves and more
than one consecutive P wave is conducted (3:2 or bet-
ter). When this occurs, the level of the AV block may be
localized.
When conduction improves and 2:1 block is seen in as-
sociation with type I block, the block is AV nodal (Fig.
8.28).
When conduction improves and 2:1 block is seen in
association with type II block (fixed PR intervals
and wide QRS complexes), the block is infranodal
(Fig. 8.29).
Acute MI and AV block: When 2:1 block complicates
acute MI, the location of the infarct is helpful in identi-
fying the level of the AV block. If the infarct is inferior
and the QRS complexes are narrow, the AV block is at
the level of the AV node (Fig. 8.30).
Advanced Second-Degree AV Block: 3:1
and Higher
Advanced second-degree AV block: When the AV
block is 2:1, 3:1, 4:1, or higher, the AV block cannot be
classified as type I or type II because only a single P
wave is conducted (2:1 block) or two or more consecu-
tive P waves are blocked (3:1 AV block or higher).
These are examples of advanced second-degree AV
block (Figs. 8.318.33).
The conduction ratio refers to the number of P waves
that are blocked before a P wave is conducted. Thus, a
3:1 conduction ratio implies that of three consecutive P
waves, only one is conducted.
Advanced AV block with narrow QRS complexes may
be nodal or infranodal (Figs. 8.31 and 8.32). When the
QRS complexes are wide, the block is almost always in-
franodal (Fig. 8.33).
ECG Findings of Advanced Second-Degree
AV Block
1. Advanced or high-grade AV block is a form of second-
degree block where two or more consecutive P waves are not

Figure 8.27: 2:1 Second-Degree Atrioventricular (AV) Block with Wide QRS Complexes. The rhythm
is 2:1 AV block similar to Figure 8.26. In this example, the QRS complexes are wide because of right bundle branch
block, a sign of distal conduction system disease. This type of 2:1 block can be infranodal occurring at the level of
the bundle branches although AV nodal block is also possible. The stars point to the nonconducted P waves.
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94 Chapter 8

#1

#2

Figure 8.28: 2:1 Second-Degree Atrioventricular (AV) Block Occurring with AV Wenckebach.
Rhythm strip 1 shows 2:1 AV block. Rhythm strip 2 is from the same patient taken several minutes later showing
3:2 AV Wenckebach. Because 2:1 AV block is seen in association with classical AV Wenckebach with narrow
complexes, the 2:1 block is at the level of the AV node.The stars identify the blocked P waves.

conducted as in 3:1, 4:1, or 5:1 AV block. A 2:1 AV block is also
included as a form of advanced second-degree AV block be-
cause only a single P wave is conducted.
2. The QRS complexes may be narrow or wide.
3. The long pauses are often terminated by escape beats.
Mechanism
Advanced second-degree AV block can occur at the level of
the AV node (AV nodal block). It can also occur more distally
at the level of the His-Purkinje system (infranodal block).
AV nodal block: Advanced second-degree AV block oc-
curring at the AV node may have narrow or wide QRS
complexes, although typically the QRS complexes are
narrow.
Infranodal block: Advanced second-degree AV block
can occur at the level of the bundle of His or more distally
at the level of the bundle branches. The QRS complexes
may be narrow or wide, although typically the QRS com-
plexes are wide.
n Bundle of His: Advanced second-degree block can
occur at the level of the bundle of His, but this type of
AV block (intra-His block) is uncommon. The QRS
complexes are narrow.
n Bundle branches: When the block is at the level of the
bundle branches, the baseline ECG will show wide
QRS complexes because of right or left bundle branch
block.
Ventriculophasic sinus arrhythmia may occur when there is
2:1 AV block. The P-P interval with a QRS complex is shorter
than the P-P interval without a QRS complex. The P-P inter-
val with a QRS complex has stroke volume that can stretch the
carotid baroreceptors, causing vagal inhibition that is most
pronounced in the next cardiac cycle. This results in a longer
P-P interval in the cardiac cycle without a QRS complex.
Clinical Significance
It is a common mistake to classify 2:1 AV block always as a
type II block because the PR interval is fixed. Because there is

#1

1.4 sec 1.4 sec

#2

#3

Figure 8.29: 2:1 Second-Degree Atrioventricular (AV) Block with Wide QRS
Complexes. The rhythm strips labeled 1, 2, and 3 are continuous. Rhythm strip1 shows 2:1
AV block; rhythm strip 2 shows three consecutively conducted P waves with a classical Mob-
itz type II pattern. The PR interval is fixed and the R-R interval is also fixed. In rhythm strip 3,
2:1 AV block is again present. The transient occurrence of Mobitz type II AV block, which is an
infranodal block, suggests that the 2:1 block is infranodal, occurring at the level of the bundle
branches. The stars identify the blocked P waves.
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Atrioventricular Block 95

Figure 8.30: Two to One Atrioventricular (AV) Block and Acute Inferior Myocardial Infarction
(MI). Twelve-lead electrocardiogram showing 2:1 AV block with narrow QRS complexes occurring as a complica-
tion of acute inferior MI. The stars identify the P waves that are not conducted. The presence of acute inferior MI
with narrow QRS complexes localizes the AV block at the level of the AV node.

3:1 AV Block

Figure 8.31: Advanced Second-Degree Atrioventricular (AV) Block. The rhythm

is normal sinus with 3:1 AV block (bracket). The QRS complexes are narrow. When the QRS
complexes are narrow, the block may be nodal or infranodal, but is usually nodal. The P
waves are marked by the arrows.

4:3 AV Wenckebach 3:2 AV Wenckebach

1 2 3 4 5 6 7 8 10 11 12 13 14

Figure 8.32: Advanced Second-Degree Atrioventricular (AV) Block. There are five consecutive P waves
(labeled 4 to 8) that are not conducted.The pause is terminated by a junctional escape complex (arrow). Beats 1 to 4
and 10 to 12 show classical AV Wenckebach with gradual lengthening of the PR interval followed by a P wave that
is not conducted (beats 4 and 12). The PR interval shortens immediately after the pause (beat 13). The presence of
classical AV Wenckebach with narrow complexes indicates that the advanced AV block is at the level of the AV
node. The presence of an AV junctional escape complex also indicates that the block is AV nodal.
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96 Chapter 8
Figure 8.33: Advanced (3:1) Second-Degree Atrioventricular (AV) Block. When advanced second-
degree AV block has wide QRS complexes, the block is almost always infranodal. In this example, one bundle branch
has a fixed blocked and the other bundle branch is intermittently blocked, resulting in nonconducted P waves. The
arrows identify the P waves.
only a single conducted P wave and the next P wave is
blocked, there is only one PR interval that can be meas-
ured. Thus, it is not possible to classify 2:1 block as type I
or type II. At least two consecutive P waves should be con-
ducted to differentiate type I from type II block. A 2:1 AV
block is an example of advanced AV block. It is preferable
to leave the diagnosis of 2:1 block simply as 2:1 second-de-
gree AV block without specifying that the AV block is type
I or type II.
Infranodal block implies a more serious conduction abnor-
mality than AV nodal block. The location of the conduction
abnormality can be identified as nodal or infranodal by the
following features.
When 2:1 AV block or a higher conduction ratio, such as
3:1 or 4:1 AV block is associated with AV Wenckebach
with narrow QRS complexes, the block is at the level of
the AV node.
When 2:1 AV block or a higher conduction ratio is associ-
ated with type II block with a fixed PR interval and wide
QRS complexes, the block is below the AV node.
When advanced AV block is associated with the use of
pharmacologic agents that can block the AV node (beta
blockers, calcium blockers, or digitalis), the block is AV
nodal.
When advanced AV block occurs in the setting of an acute
infarction:
n If the infarct is inferior, the block is AV nodal. The
QRS complexes are narrow.
n If the infarct is anterior, the block is infranodal. This is
usually associated with wide QRS complexes.
If the AV block is infranodal, evidence of infranodal dis-
ease, such as right or left bundle branch block, should be
present. In general, advanced AV block with wide QRS
complexes with a conduction ratio of 3:1 or higher com-
monly involves the His-Purkinje system.
If an escape beat is present, the origin of the escape com-
plex may be helpful in localizing the level of the AV
block.
n If the escape beat has a narrow QRS complex, the
block is AV nodal. A block within the bundle of His
(intra-His) is possible but uncommon.
n If the escape complex is wide, the AV block is usually
infranodal.
n The causes of advanced second-degree AV block are
identical to those of types I and II AV block.
Treatment
Advanced AV block, including 2:1 AV block at the level of the
AV node, is usually transient with a good prognosis. Therapy is
not required if the patient is asymptomatic and the heart rate
exceeds 50 bpm. However, if symptoms related to bradycardia
occur, atropine is the drug of choice (see Treatment of Com-
plete AV Block in this Chapter). Atropine is not effective if the
AV block is infranodal. An intravenous adrenergic agent such as
isoproterenol, 2 to 10 mcg/minute or epinephrine 2 to 20
mcg/minute, may be given emergently as a continuous infusion
until a transvenous (or transcutaneous) pacemaker becomes
available. The dose is titrated according to the desired heart rate
(see Treatment of Complete AV Block in this Chapter).
In patients where the AV block is not reversible, a permanent
pacemaker is indicated. The following are indications for in-
sertion of permanent pacemaker in advanced second-degree
AV block according to the ACC/AHA/HRS guidelines.
Symptomatic patients: For patients with advanced
second-degree AV block who have symptoms or ventricular
arrhythmias related to the bradycardia, insertion of a per-
manent pacemaker is a Class I recommendation regard-
less of the anatomic level of the AV block.
Asymptomatic patients: In asymptomatic patients
with advanced second-degree AV block, permanent pac-
ing is a Class I indication in the following conditions re-
gardless of the site of the AV block.
n Patients with arrhythmias and other medical condi-
tions that require drugs that can cause symptomatic
bradycardia.
n Documented asystole 3.0 seconds or any escape rate
40 bpm in patients with sinus rhythm who are
awake and asymptomatic.
n In patients with atrial fibrillation with 1 pauses of
5 seconds.
n After catheter ablation of the AV junction.
n Postcardiac surgery AV block that is not expected to
resolve.
n Neuromuscular diseases including myotonic muscular
dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and
peroneal muscular atrophy with or without symptoms.
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Atrioventricular Block 97

Figure 8.34: Third-Degree or Complete Atrioventricular (AV) Block. In complete AV block, it is

not possible for any atrial impulse to propagate to the ventricles, therefore only P waves (and no QRS com-
plexes) will be present. Unless the ventricles are activated by another impulse originating below the level of
the block, the ventricles will remain asystolic, resulting in syncope or sudden death.

n During exercise in the absence of myocardial ischemia.
n Asymptomatic patients with advanced AV block at the
infranodal level diagnosed during electrophysiologic
study for other indications. This is a Class IIa recom-
mendation.
n AV block that is expected to resolve or unlikely to
recur such as those resulting from drug toxicity, Lyme
disease, or during hypoxia related to sleep apnea in the
absence of symptoms is a Class III recommendation.
Prognosis
The prognosis of high-grade AV block depends on the etiol-
ogy of the AV block. Patients with isolated advanced AV
Localizing the AV Block
block resulting from degenerative disease of the conduction
system may have the same prognosis as those without ad-
vanced AV block after a permanent pacemaker is implanted.
Third-Degree or Complete AV Block
Complete or third-degree AV block: In complete or
third-degree AV block, there is complete failure of all
atrial impulses to conduct to the ventricles; therefore,
only P waves will be present (Fig. 8.34). These P waves
are unable to reach the ventricles because they are
blocked or interrupted somewhere in the AV conduc-
tion system (Fig. 8.35). Unless an escape rhythm
comes to the rescue, the ventricles will remain asys-
tolic and the patient will develop syncope or die
suddenly.
The origin of the escape rhythm will depend on the lo-
cation of the AV block. These escape complexes are
completely independent from the sinus P waves, result-
ing in complete dissociation between the P waves and
the QRS complexes.
Complete AV block may occur at the level of the AV
node or it may be infranodal, occurring below the AV
node anywhere in the His bundle, bundle branches,
and more distal conduction system.
AV nodal block: If complete AV block occurs at the
level of the AV node, a junctional escape rhythm usu-
ally comes to the rescue.
AV junctional escape rhythm: The AV junction in-
cludes the AV node all the way down to the bifurca-

Sinus Node

Atria

AV Node
AV
Bundle of His Conduction
System
Bundle Branches

Ventricles

Figure 8.35: Complete Atrioventricular (AV) Block. Complete AV block can

occur anywhere along the AV conduction system. It can occur at the AV node or bun-
dle of His. It can involve both bundle branches simultaneously or the right bundle
plus both fascicles of the left bundle branch. When complete AV block is present, the
location of the conduction abnormality should always be identified because
prognosis will depend on the location of the AV block.
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98 Chapter 8
Sinus Node
Atria
AV Junctional
Escape Rhythm
Ventricles
Figure 8.36: Complete Atrioventricular (AV) block with Narrow QRS Complexes. If com-
plete AV block occurs at the level of the AV node, a junctional escape rhythm (star) comes to the
rescue. The QRS complexes are narrow because the impulse originates above the bifurcation of the
bundle of His and can activate both ventricles simultaneously. Arrows point to sinus P waves, which
are completely dissociated from the QRS complexes.
tion of the bundle of His. The escape rhythm usually
originates below the AV node at its junction with the
bundle of His. Any impulse originating above the bi-
furcation of the bundle of His such as a junctional
rhythm can activate both ventricles simultaneously,
resulting in a narrow QRS complex (Fig. 8.36). The
presence of AV junctional rhythm indicates that the
block is at the level of the AV node. If the AV junction
is suppressed or inhibited or is structurally abnormal,
a ventricular escape rhythm may come to the rescue.
Ventricular escape rhythm: A ventricular escape
rhythm has wide QRS complexes because it origi-
nates below the bifurcation of the bundle of His
(Fig. 8.37). The presence of a ventricular escape
rhythm usually indicates that the block is infran-
odal, although the AV block may occasionally occur
at the level of the AV node.
Infranodal block: When the block is infranodal, it
usually occurs at the level of the bundle branches or
fascicles. It can also occur at the level of the bundle of
His, although a block at the level of the bundle of His
(intra-His block) is rare. When the block is infranodal,
only a ventricular escape rhythm with wide QRS com-
plexes can come to the rescue. The QRS complexes are
wide because the impulse originates below the bifurca-
tion of the bundle of His; thus, the ventricles are not
activated simultaneously. Conduction of the impulse is
delayed and is transmitted from one ventricle to the
other by muscle cell to muscle cell conduction. A junc-
tional escape rhythm cannot come to the rescue be-
cause it will not be able to continue down the conduct-
ing system and will not be able to reach the ventricles.
The origin of the escape rhythm is helpful in localizing
the level of the AV block as shown in Figure 8.19.
AV Block at the AV Node
The presence of an acute MI is useful in localizing the
AV block.
Acute anterior MI: When complete AV block oc-
curs in the setting of an acute anterior MI, the AV
block is infranodal. The AV block is frequently pre-
ceded by left or right bundle branch block and the
escape rhythm is ventricular (Fig. 8.38).
Acute inferior MI: When complete AV block occurs
in the setting of an acute inferior MI, the AV block is
at the AV node (Fig. 8.39).
Figure 8.39 shows acute inferior MI with complete AV
dissociation. The presence of acute inferior MI with
junctional rhythm (narrow QRS complexes) suggests
that the AV block is at the level of the AV node.
Although a junctional escape rhythm points to the AV
node as the site of the AV block, a ventricular escape
rhythm does not indicate that the AV block is always
infranodal. In Figure 8.40, the first three escape com-
plexes are ventricular, suggesting an infranodal loca-
tion of the AV block. The last three escape complexes,
however, are narrow and are junctional in origin. This
makes an infranodal block highly unlikely. The pres-
ence of junctional escape complexes therefore suggests
that the AV block is AV nodal.
The surface ECG is an excellent diagnostic tool in lo-
calizing the level of AV block, making electrophysio-
logic testing rarely necessary. However, when the level
of AV block remains uncertain, intracardiac ECG may
be used to verify the exact location of the AV conduc-
tion abnormality.
Intracardiac ECG can be obtained by inserting an elec-
trode catheter into a vein and advancing it to the right
ventricle at the area of the bundle of His.
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A B

Junctional Escape Rhythm

AV Block at the AV Block at the

Bundle of His Bundle Branches or
Fascicles
Ventricular Escape Rhythm

Figure 8.37: Complete Atrioventricular (AV) Block with Wide QRS Complexes.
The atrial impulses, identified by the arrows, cannot conduct to the ventricles because of
complete AV block, which can occur at the level of the bundle of His (A) or bundle branches
and fascicles (B). A block at the level of the bundle of His is possible but is rare. When there is
infranodal block, the QRS complexes are wide because the escape rhythm originates from
the ventricles (star). It is not possible for a junctional escape rhythm (asterisk) to come to the
rescue because the origin of the impulse is proximal to the block and will not be able to
propagate to the ventricles.

A: Acute anteroseptal MI: Figure 8.38: Atrioventricular

(AV) Block Complicating
Acute Anterior Myocardial In-
farction (MI). Electrocardiogram
(ECG) A shows acute anteroseptal
MI complicated by first-degree AV
block, right bundle branch block,
and left anterior fascicular block.
ECG B shows complete AV dissoci-
ation. The P waves are marked by
the arrows.

B: Complete AV dissociation:

99
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100 Chapter 8

Figure 8.39: Acute Inferior Myocardial Infarction (MI) with Complete Atrioventricular (AV) Dissoci-
ation. When acute inferior MI is accompanied by AV dissociation, the AV block is at the level of the AV node. The
arrows identify the P waves. Note also that the escape rhythm is AV junctional with narrow QRS complexes.

Surface ECG: When the atria and ventricles are ac-
tivated by the sinus impulse, the surface ECG
records a P wave, which corresponds to atrial activa-
tion and a QRS complex, which corresponds to ven-
tricular activation (Fig. 8.41A).
Intracardiac ECG: The intracardiac ECG will be
able to record not only atrial (A) and ventricular (V)
activation, which corresponds to the P wave and
QRS complex in the surface ECG, but can also
record activation of the His bundle (H), which is
represented as a deflection between the P wave and
the QRS complex (Fig. 8.41B).
Intracardiac ECG or His Bundle Recording
The His deflection allows the PR or A-V interval to be
divided into two components:
A-H interval: This represents conduction between
atria and His bundle corresponding to the transmis-
sion of the impulse across the AV node.
H-V interval: This represents conduction between
the His bundle and ventricles corresponding to the
transmission of impulse in the bundle branches and
distal conduction system.
When an atrial impulse is blocked and is not followed
by a QRS complex, the intracardiac recording can lo-
calize the AV block.
AV nodal: If the atrial impulse is not followed by
His deflection (and ventricular complex), the AV
block is AV nodal (Fig. 8.42A).
Infranodal: If the atrial impulse is followed by His
spike but not a ventricular complex, the AV block is
infranodal (Fig. 8.42B).
Intra-His: The atrial impulse can be blocked at the
level of the bundle of His (intra-His block), al-
though this is rare.
In complete AV block, the ventricular rate should al-
ways be slower than the atrial rate and not the other way
around. The ventricles and AV conduction system
should be given enough time to recover so that the atrial

Figure 8.40: Complete Atrioventricular (AV) Block. The presence of ventricular escape rhythm does not
indicate that the block is always infranodal.The rhythm strip shows complete AV block.The QRS complexes are
marked by the stars. The first three complexes are wide and represent ventricular escape complexes suggesting
that the AV block is infranodal. The last three complexes, however, are narrow, representing junctional rhythm that
makes an infranodal block unlikely.
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Atrioventricular Block 101

QRS
P
A

Surface
ECG
HV H H H
A
B
Intracardiac

Figure 8.41:The Surface Electrocardiogram (ECG) and Intrac-

ardiac Recording. The surface ECG is capable of recording only the P
wave and the QRS complex, whereas an intracardiac study is capable of
recording not only atrial (A) and ventricular (V) activation but also that of
the His (H) bundle. The presence of the His deflection allows the PR inter-
val to be divided into two main components: the A-H interval (atrium to
His interval), which represents conduction through the AV node (normal
60 to 125 milliseconds) and H-V interval, which represents conduction
through the distal conduction system between the His bundle and ventri-
cles (normal, 35 to 55 milliseconds).

impulse will not find the ventricles refractory. Thus, the

ventricular rate should not only be slower than the
atrial rate but should be 50 bpm, usually in the low to
mid-40s before the AV block is considered complete.
Complete AV block can occur regardless of the atrial
rhythm, which could be normal sinus (Fig. 8.43), atrial
flutter (Fig. 8.44), or atrial fibrillation (Fig. 8.45).
QR
P
A
A HV A Concealed conduction: Concealed conduction is com-
B A H
Figure 8.42: Intracardiac Electrocardiogram (ECG).
(A) Atrioventricular (AV) block at the level of the AV node. The
surface ECG shows a P wave that is not conducted (arrow). The
intracardiac ECG shows an atrial deflection (A) that is not
followed by a His deflection thus the AV block is AV nodal. (B) AV
block involving the distal conduction system.The surface ECG
shows a P wave that is not conducted (arrow). Intracardiac ECG
shows an atrial deflection followed by a His deflection but not a
ventricular deflection suggesting that the AV block is distal to
the His bundle at the bundle branches and distal conduction
system. A, atrial complex; H, His spike; V, ventricular complex.
Common Mistakes in AV Block
Sinus arrest: When only QRS complexes are present and
atrial activity is absent (no P waves), the rhythm is sinus
arrest and not complete AV block (Figs. 8.46 and 8.47).
Complete AV block versus advanced second-degree AV
block: In complete AV block, there should be complete
dissociation between the P waves and the QRS com-
plexes. If a single P wave captures a QRS complex, the
AV block is no longer complete (Fig. 8.48).
Blocked Premature Atrial Complexes (PACs): Blocked
premature atrial complexes may be mistaken for non-
conducted sinus P waves and mistaken for second-
degree AV block (Fig. 8.49).
monly mistaken for AV block. Concealed conduction indi-
cates that a previous impulse had infiltrated the conduc-
tion system. This will have an effect on the next impulse.
Figure 8.50 shows a sinus P wave (star) that is not followed
by a QRS complex. This can be mistaken for second-de-
gree AV block. Although a nonconducted sinus P wave is
obvious, there is a premature ventricular impulse preced-
ing the P wave. This premature impulse depolarized not
only the ventricles, but also the AV conduction system ret-
rogradely, rendering the AV node refractory. The effect of
the premature impulse on the conduction system is not
apparent until the arrival of the next sinus impulse, which
is unable to conduct to the ventricles because the AV node
is still refractory. This is an example of concealed conduc-
tion and not second-degree AV block. Figure 8.51 is a sim-
ilar example of concealed conduction showing sinus P
waves that are not conducted (arrows). The blocked P
waves are preceded by premature ventricular complexes.
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102 Chapter 8

Figure 8.43: Complete Atrioventricular (AV) Block. The rhythm is normal sinus with a rate of 96 beats per
minute.The ventricular rate is 26 beats per minute (arrows). Note that the P waves are completely dissociated and
have no relation to the QRS complexes because complete AV block. Note also that the atrial rate is faster than the
ventricular rate.

Figure 8.44: Complete Atrioventricular (AV) Block. The rhythm is atrial flutter.The ventricular rate is slow
and regular and is 30 beats per minute because of complete AV block. The presence of wide QRS complexes indi-
cates that the escape rhythm is ventricular in origin and suggests that the block is infranodal.

Figure 8.45: Complete Atrioventricular (AV) Block. The rhythm is atrial fibrillation with complete AV block
with a slow ventricular rate of approximately 33 beats per minute.The QRS complexes are wide and regular,
suggesting that the escape rhythm is ventricular in origin.This favors an infranodal block. In atrial fibrillation, the
R-R intervals are irregularly irregular. When the R-R intervals suddenly become regular, complete AV block should
always be considered.

Figure 8.46: This is Not Complete Atrioventricular (AV) Block. Because there is no atrial activity,
atrioventricular block is not present. The underlying mechanism is due to complete absence of sinus node activity
(sinus arrest) because of sick sinus syndrome. The sinus arrest is terminated by a ventricular escape complex.

Figure 8.47: Sinus Node Dysfunction Mistaken for Complete Atrioventricular Block. Again, there is
no evidence of atrial activity; therefore, atrioventricular (AV) block is not present. The rhythm is AV junctional with a
slow ventricular rate of 39 beats per minute because of sick sinus syndrome.
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Atrioventricular Block 103

1.56 s 1.56 s 1.04 s 1.56 s 1.56 s

Figure 8.48: Advanced Atrioventricular Block (AV) Mistaken for Complete AV Block. The
P wave with a circle captures a QRS complex resulting in sudden shortening of the R-R interval to 1.04
seconds. If one P wave is able to capture the ventricles as shown, the atrioventricular (AV) block is not
complete. This is an example of advanced but not complete AV block.

Figure 8.49: Blocked Premature Atrial Complexes (PACs) Resembling Second-Degree Atrioventric-
ular (AV) Block. The blocked PACs are marked by the arrows. Note that the P waves are premature and are
followed by pauses. These nonconducted premature atrial complexes may be mistaken for sinus P waves and the
rhythm can be mistaken for second-degree AV block.

Figure 8.50: Concealed Conduction. The rhythm strip shows a sinus P wave without a QRS complex (star),
which can be mistaken for second-degree atrioventricular (AV) block. Preceding the sinus P wave is a premature
ventricular complex (arrow) that retrogradely penetrated the AV conduction system, making the AV node refrac-
tory.Thus, the next sinus impulse was not conducted.This is an example of concealed conduction and not second-
degree AV block.

Figure 8.51: Concealed Conduction. Sinus P waves without QRS complexes (arrows) are noted only after
every ventricular ectopic impulse. This is an example of concealed conduction and not second-degree atrioventric-
ular block.
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104 Chapter 8

TABLE 8.1

Indications for Insertion of Permanent Cardiac Pacemakers in Patients with Acquired

AV Block in Adults
Third-degree and advanced
second-degree AV block at
any anatomic level
Type II second-degree AV block
Type I second-degree AV block
Marked first-degree AV block
From the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. All the above recommendations for perma-
nent pacemaker insertion are Class I indications unless specified.
a
Neuromuscular diseases include myotonic muscular dystrophy, Erb dystrophy (limb-girdle), peroneal muscular atrophy, and Kearns-Sayre syndrome.
AV, atrioventricular.
Symptomatic individuals: Bradycardia causes symptoms (including heart failure)
or ventricular arrhythmias presumed to be due to AV block.
Asymptomatic individuals:
Arrhythmias and other medical conditions that require drug therapy that results in
symptomatic bradycardia.
Documented asystole of 3.0 seconds or escape rate is 40 beats per minute in
awake or asymptomatic patients in sinus rhythm.
Atrial fibrillation and bradycardia of 1 or more episodes of 5 seconds duration.
Heart rate 40 beats per minute when awake but with persistent third-degree AV
block with cardiomegaly or left ventricular dysfunction.
Second or third-degree AV block during exercise in the absence of myocardial
ischemia.
After cardiac procedures:
Postablation of the AV junction
AV block occurring after cardiac surgery that is not expected to resolve
AV block Associated with neuromuscular diseases:a
The patient may be symptomatic or asymptomatic
Symptomatic patients:
Symptomatic patients because of bradycardia.
Asymptomatic patients:
Type II second-degree AV block with wide QRS complexes.
Type II second-degree AV block with narrow QRS complexes (Class IIa).
Symptomatic individuals:
Symptoms of low output and hypotension because of bradycardia regardless of the
level of AV block.
Patient may not be bradycardic but symptoms are similar to pacemaker syndrome
(Class IIa).
Asymptomatic individuals:
AV block at or below the level of the bundle of His usually diagnosed during electro-
physiological study performed for other indications (Class IIa).
Patients with neuromuscular disease:a
Patients may be symptomatic or asymptomatic (Class IIb).
Symptomatic individuals:
Symptoms of low output and hypotension similar to pacemaker syndrome in pa-
tients with left ventricular dysfunction or congestive heart failure. The symptoms
should be improved by temporary AV pacing (Class IIa).
Patients with neuromuscular disease:a
Patients may be symptomatic or asymptomatic (Class IIb).

Figure 8.52 summarizes diagrammatically the different patients with acquired AV block according to the
types of AV block. ACC/AHA/HRS guidelines (see Table 8.1).

Indications for Permanent Pacing ECG Findings of Complete AV Block

in AV Block 1. In complete AV block, there is complete failure of the atrial im-
pulses to capture the ventricles.
Unless specified, the following are Class I indications 2. Only P waves will be present. Unless an escape rhythm comes
for implantation of permanent pacemakers in adult to the rescue, ventricular asystole will occur.
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Atrioventricular Block 105

Summary of the Different Types of AV Block Figure 8.52: Atrioventricular

(AV) Block. The figure summarizes
the different types of AV block.
1 AV Block

Type I 2 AV Block

Type II 2 AV Block

Advanced 2:1
2 AV Block

Advanced 3:1
2 AV Block

Complete AV
Block (AV Nodal)

Complete AV
Block (Infranodal)

Complete AV
Dissociation
(Junctional
Tachycardia)

3. The escape rhythm (the QRS complexes) can be narrow or
wide.
4. The P waves and QRS complexes are completely dissociated.
5. The ventricular rate should be slower than the atrial rate and
should be 50 bpm, usually in the mid- to low 40s.
Mechanism
The intraventricular conduction system contains special cells
with automatic properties that are capable of becoming
pacemakers. These cells are called latent pacemakers because
their rate of discharge is slower than the sinus node and do
not become manifest because they are depolarized by the
propagated sinus impulse. When the sinus impulse is
blocked or when there is significant slowing of the sinus
node, these latent pacemakers can become the dominant
pacemaker of the heart. Cells in the middle portion of the AV
node called the N region do not have automatic properties
and cannot become pacemakers. Cells at the upper portion
of the AV node at its junction with the atria (AN region),
lower portion of the AV node at its junction with the bundle
of His (NH region) and His-Purkinje system have pacemak-
ing properties. Cells with automatic properties that are lo-
cated higher in the conduction system (closer to the AV
node) have higher rates than cells that are located more dis-
tally. Thus, the intrinsic rate of the AV junction is 40 to 60 bpm
and cells that are located more distally in the His-Purkinje
system have slower rates of 20 to 40 bpm.
Complete AV block can occur anywhere in the AV conduc-
tion system. It can occur at the level of the AV node, bundle
of His, both bundle branches, or the right bundle branch in
combination with block involving both fascicular branches
of the left bundle branch. If complete AV block is present,
the sinus impulse will not be able to reach the ventricles be-
cause the AV conduction system is the only pathway by
which the sinus impulse can reach the ventricles. This will
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106 Chapter 8
result in syncope or sudden death unless an ectopic impulse
comes to the rescue and initiates a ventricular rhythm. The
escape rhythm has to originate below the level of the AV
block. Thus, if the AV block is at the AV node, a junctional
escape rhythm with narrow QRS complex usually comes to
the rescue, and if the AV block is at the level of the His-
Purkinje system, a ventricular escape rhythm with wide QRS
complex is usually the escape mechanism. The presence of
complete AV block is not certain unless the ventricles and
AV conduction system are given enough time to recover
from the previous impulse. For this to occur, the ventricular
rate should be slower than the atrial rate and should be 50
bpm, usually in the mid- to low 40s.
Clinical Implications
Complete AV block can occur suddenly and can cause syn-
cope or sudden death. The location of the AV block has prog-
nostic significance and should be localized in all patients
with AV block. The origin of the escape rhythm as well as the
clinical setting in which the AV block occur are useful in lo-
calizing the AV block.
If the escape rhythm is AV junctional, the block is at the
level of the AV node. In infranodal block, the escape
rhythm is always ventricular.
The presence of bundle branch block before the onset of
complete AV block suggests that there is distal conduction
disease and favors an infranodal block.
If the patient is taking pharmacologic agents that block
the AV node, such as digitalis, calcium channel blockers,
or beta blockers, the block is AV nodal.
When complete AV block occurs in the setting of an acute
inferior MI and the QRS complexes are narrow, the AV
block is AV nodal.
When complete AV block occurs in the setting of acute an-
terior MI, the AV block is infranodal. When the AV block is
infranodal, bundle branch block is usually present.
There are multiple causes of complete AV block. Complete AV
block may be congenital, occurring at birth, or advanced age
resulting from calcification of the aortic ring and mitral annu-
lus (also called Lev disease) and fibrosis or sclerodegenerative
changes involving the conduction system (also called Lengre
disease). It could also be due to acute MI, inflammation of the
conduction system as in Lyme disease, diphtheria, or Chagas
disease, or from infiltrative diseases such as sarcoid or amyloid,
hypothyroidism, and neuromuscular diseases. It could also be
due to drugs that block the AV node or distal conducting sys-
tem or during intracardiac surgery or ablation procedures.
Physical examination of a patient with complete AV block will
show cannon A waves in the jugular neck veins, variable inten-
sity of the first heart sound, and variable pulse volume. This is
similar to the physical findings of ventricular tachycardia (see
Chapter 22, Wide Complex Tachycardia). These physical find-
ings are due to the presence of complete AV dissociation.
Cannon A waves in the neck: When there is complete
AV dissociation, there is no relationship between atrial
and ventricular contraction; thus, atrial contraction often
occurs during systole when the tricuspid and mitral valves
are closed, resulting in prominent jugular neck vein pul-
sations called cannon A waves. These cannon A waves oc-
cur intermittently, only when atrial and ventricular con-
tractions are simultaneous.
Varying intensity of the first heart sound: The inten-
sity of the first heart sound depends on the position of
the mitral and tricuspid valves at the onset of systole.
When the valves are wide open, the first heart sound is
markedly accentuated because of the wide distance the
leaflets have to travel to their closure points. On the other
hand, when the valves are near their coaptation points,
the first heart sound will be very soft and hardly audible
because the leaflets are almost in a semiclosed position at
the onset of systole. During atrial contraction correspon-
ding to the P wave in the ECG, the mitral and tricuspid
leaflets are pushed wide open toward the ventricles away
from their closure points. If this is immediately followed
by ventricular contraction (as when the PR interval is
short), closure of the mitral and tricuspid leaflets will be
loud and often booming. On the other hand, if atrial
contraction is not immediately followed by ventricular
contraction (as when the PR interval is unduly pro-
longed), the closure of the leaflets will be soft or inaudi-
ble because the leaflets are allowed to drift back to a
semiclosed position at the onset of ventricular contrac-
tion. Because the PR interval is variable when there is
complete AV dissociation, the intensity of the first heart
sound will also be variable.
Varying pulse volume: When the P waves and the QRS
complexes are completely dissociated, some ventricular
beats will be preceded by atrial contraction, whereas other
beats are not. When a P wave precedes a QRS complex,
ventricular filling is augmented, resulting in a larger
stroke volume, whereas QRS complexes without preced-
ing P waves will have a lower stroke volume.
Jugular venous pulsations: The jugular venous pulsations
may be useful in the diagnosis of cardiac arrhythmias. In
1899, Wenckebach described the second-degree AV block
that bears his name without using an ECG by examining
jugular pulse tracings. The jugular pulse consists of three
positive waves (a, c, and v waves) and two negative waves (x
and y descents). To identify these waves and descents at bed-
side, the patient should be positioned properly and lighting
should be adequate. The internal jugular veins lie deep be-
hind the sternocleidomastoid muscle; thus, the venous col-
umn is not normally visible unless there is increased venous
pressure because of right heart failure. The internal jugular
pulsations, however, can be identified because they are trans-
mitted superficially to the skin. Simultaneous auscultation of
the heart or palpation of the radial pulse or opposite carotid
artery is useful in timing the pulsations.
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Jugular versus carotid pulsations: If there is difficulty
in differentiating jugular venous from carotid arterial
pulsations, the patient should be positioned more verti-
cally upright because the venous pulse may disappear,
whereas the arterial pulse does not disappear with any po-
sition. The venous pulse has two waves, with an inward
motion corresponding to the x and y descents, whereas
the arterial pulse has a single wave with an outward mo-
tion. If there is still doubt whether the pulse is venous or
arterial, the base of the neck above the clavicle should be
compressed. If the pulsation is venous, the pulse will dis-
appear. Deep inspiration may enhance the venous pulsa-
tions, whereas the carotid pulse is not altered by pressure
or by inspiration.
n The a wave: The a wave corresponds to the P wave
in the ECG and is due to the rise in jugular venous
pressure during atrial contraction. There is slight me-
chanical delay in the transmission of the atrial pulse to
the neck; thus, the peak of the a wave usually coin-
cides with the onset of the first heart sound. The a
wave is prominent when there is increased resistance
to the flow of blood to the right ventricle, as when
there is tricuspid stenosis, right ventricular hypertro-
phy, pulmonic stenosis, or pulmonary hypertension. It
is also prominent when there is left ventricular hyper-
trophy because the septum is shared by both ventri-
cles. The a wave is absent if there is atrial fibrillation
or the rhythm is AV junctional.
n The x descent: The x descent is the most conspicuous
jugular motion occurring immediately after the a
wave and is due to atrial relaxation and downward
motion of the tricuspid annulus during systole.
Because timing is systolic, it is easy to identify using
the heart sounds or radial pulse. The x descent is
prominent when the a wave is prominent. It is also
prominent in constrictive pericarditis and in cardiac
tamponade. The x descent is absent when there is no
a wave, such as when there is AV junctional rhythm
or atrial fibrillation.
n The c wave: The x descent in the jugular pulse is often
interrupted by the c wave, which is due to transmitted
pulsation from the carotid artery. Additionally, during
right ventricular contraction, there is bulging of the tri-
cuspid leaflets into the right atrium. The x descent con-
tinues as the x descent after the c wave. The c wave is
prominent when there is tricuspid regurgitation, often
combining with the v wave to form a prominent cv
wave. In some normal individuals, the c wave may not
be demonstrable.
n The v wave: The v wave is due to the rise in right
atrial pressure as blood accumulates in the atrium
when the tricuspid valve is closed during systole. The
peak of the v wave occurs with the onset of the sec-
ond heart sound. The v wave becomes a large cv
wave when there is tricuspid regurgitation. It is also
Atrioventricular Block 107
prominent when there is increased right atrial pres-
sure resulting from cardiomyopathy or increased vol-
ume due to atrial septal defect.
n The y descent: The y descent follows the downslope of
the v wave and is due to the fall in right atrial pressure
when the tricuspid valve opens during diastole. The y
descent occurs after the second heart sound or after the
radial pulse and is prominent in restrictive cardiomy-
opathy, constrictive pericarditis, right ventricular in-
farction, and tricuspid regurgitation. The y descent be-
comes diminished when there is tricuspid stenosis.
The jugular neck vein pulsations may be helpful in the di-
agnosis of certain arrhythmias:
n First-degree AV block: When the PR interval is pro-
longed, the a to c interval is wide.
n Type I second-degree AV block or AV Wenckebach:
In AV Wenckebach, the interval between the a wave
and c wave gradually widens until the a wave is not
followed by a v wave. Additionally, as the PR interval
becomes longer, the intensity of the first heart sound
becomes softer until a dropped beat occurs.
n Type II block: When there is type II block, the interval
between the a and c waves do not vary. The inten-
sity of the first heart sound will not vary because the
PR interval is fixed.
n Other arrhythmias: Cannon A waves are intermittently
present when there is complete AV dissociation resulting
from complete AV block or ventricular tachycardia.
Cannon A waves are constantly present when the PR in-
terval is markedly prolonged (see First-Degree AV Block
in this chapter) when there is AV junctional rhythm,
supraventricular tachycardia from AV nodal reentry, or
AV reentry (see Chapter 16, Supraventricular Tachy-
cardia.) or when there is ventricular tachycardia with
retrograde conduction to the atria.
Treatment
If complete AV block occurs at the level of the AV node and
the patient is asymptomatic with narrow QRS complexes and
a heart rate of at least 50 bpm, no treatment is necessary,
other than further monitoring and observation. Any agent
that can cause AV block should be discontinued.
Patients with AV block may become symptomatic because
of bradycardia, which includes hypotension, altered mental
status, ischemic chest pain, or signs of heart failure and low
cardiac output. Treatment of the bradycardia includes air-
way and blood pressure support and identification of im-
mediately reversible causes of AV block, including respira-
tory causes and blood gas and electrolyte abnormalities,
hypovolemia, hypothermia, hypoglycemia, and acute coro-
nary vasospasm.
The following intravenous agents may be useful in increasing
the ventricular rate or improving AV conduction. These
agents can enhance myocardial oxygen consumption and
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108 Chapter 8
therefore should be used cautiously in the setting of acute MI
because this may result in further extension of the myocar-
dial infarct.
Atropine: The drug of choice for the treatment of
bradycardia is atropine. If there are no immediately re-
versible causes of AV block, this agent remains the drug
of choice for symptomatic bradycardia and receives a
Class IIa recommendation according to the AHA guide-
lines for cardiopulmonary resuscitation and emergency
cardiovascular care.
n Atropine 0.5 mg should be given intravenously every
3 to 5 minutes until a desired heart rate is achieved.
Complete vagal blockade is expected when a total dose
of 0.04 mg/kg or 3.0 mg is given intravenously over
2 hours.
n Atropine should not be given in doses smaller than
0.5 mg because small doses stimulate the vagal nuclei
and may enhance parasympathetic activity, resulting
in paradoxical slowing and worsening of the AV
block.
n The drug can be given intratracheally during resusci-
tation, although subcutaneous or intramuscular ad-
ministration should be avoided because these routes
of administration can also result in paradoxical
slowing.
n Atropine is not effective in patients with AV block at
the infranodal level. If the AV block is infranodal or
the bradycardia does not respond to atropine, tran-
scutaneous pacing should be instituted immediately
in patients who are symptomatic.
Alternative medications: There are other medications
that can be tried for the treatment of bradycardia if at-
ropine is not effective. These drugs are given only as alter-
native agents and receive a Class IIb recommendation ac-
cording to the AHA guidelines.
n Epinephrine: This can be given as an alternate to at-
ropine if atropine is not effective or the AV block is in-
franodal and transcutaneous pacing is not available or
has failed. This will serve as a temporizing measure be-
fore a transvenous pacemaker can be inserted. For the
treatment of bradycardia and or hypotension, the infu-
sion is prepared by adding 1 mg to 500 mL saline or
D5W and started at an initial infusion of 1 g/minute.
The recommended dose is 1 to 10 g/minute titrated
according to the desired heart rate.
n Dopamine: Dopamine may be given instead of at-
ropine or epinephrine. It can be given as monotherapy
or in combination with epinephrine. The dose is 2 to
10 g/kg/minute titrated according to the desired
heart rate.
Prognosis
n Glucagon: If atropine is not effective, glucagon has
been shown to improve symptomatic bradycardia in-
duced by drugs such as beta blockers and calcium
channel blockers. The dose is 3 mg given intra-
venously followed by infusion of 3 mg/hour if needed.
n Digibind: If complete AV block is due to digitalis ex-
cess, digitalis should be discontinued and Digibind
given as an antidote.
Transcutaneous pacing: This intervention receives a
Class I recommendation in patients who do not respond
to atropine. Transcutaneous pacing is easier to perform
than transvenous pacing and can be provided by most
hospital personnel because the procedure is noninvasive.
Transvenous pacing: Transvenous pacing should be per-
formed if transcutaneous pacing is ineffective or unsuccess-
ful or if the patient cannot tolerate transcutaneous pacing.
This procedure is invasive and takes longer to accomplish,
but provides more stable pacing.
Permanent pacing: The following are indications for inser-
tion of permanent pacemaker in complete AV block according
to the ACC/AHA/HRS guidelines. In patients in whom the AV
block is not reversible, a permanent pacemaker is indicated.
Symptomatic patients: Patients with complete AV
block at any anatomic level with symptoms related to the
bradycardia, insertion of a permanent pacemaker is a
Class I recommendation.
Asymptomatic patients: Asymptomatic patients with
complete AV block, permanent pacing is a Class I indica-
tion in the following conditions.
n Patients with arrhythmias and other medical condi-
tions that require drugs that can cause symptomatic
bradycardia.
n Documented asystole 3.0 seconds or any escape rate
40 bpm in patients with sinus rhythm who are
awake and asymptomatic.
n After catheter ablation of the AV junction.
n Postcardiac surgery AV block that is not expected to
resolve.
n Neuromuscular diseases including myotonic muscu-
lar dystrophy, Kearns-Sayre syndrome, Erb dystrophy,
and peroneal muscular atrophy with or without
symptoms.
n The recommendation is Class IIa in asymptomatic pa-
tients with complete AV block at any level with aver-
age awake ventricular rates of 40 bpm if car-
diomegaly or left ventricular dysfunction is present.
A permanent pacemaker should not be inserted if the AV
block is expected to resolve or is unlikely to recur, such as
those resulting from drug toxicity, Lyme disease, or during
hypoxia related to sleep apnea in the absence of symptoms.
These are Class III recommendations.
In patients with congenital complete AV block, the block is
almost always at the level of the AV node. The escape rhythm
is AV junctional and most patients remain stable and mini-
mally symptomatic without therapy. These patients will
eventually have permanent pacemakers implanted.
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When complete AV block is due to an acute inferior infarct, the
block is AV nodal and is usually the result of enhanced
parasympathetic activity when it occurs within 24 to 48 hours
after the acute infarct. It is usually reversible and responds to at-
ropine. If the onset of the AV block is after the second or third
day, it is usually the result of continuing ischemia or structural
damage to the AV node. Although the prognosis is good be-
cause the level of the block is AV nodal, inferior infarction with
complete AV block generally indicates a larger infarct than one
without AV block and therefore has a higher mortality.
When complete AV block occurs in the setting of an acute
anterior MI, the block is almost always infranodal and is very
often preceded by bundle branch block. The mortality re-
mains high even if a pacemaker is inserted because anterior
infarct associated with AV block is usually extensive.
The prognosis will also depend on the level of the AV block.
AV nodal block: AV nodal block has a better prognosis
than an infranodal block because AV nodal block is usu-
ally reversible and a permanent pacemaker is often not
needed. The AV junction can come to the rescue and has
the highest firing rate among all potential pacemakers be-
low the AV node. AV junctional rhythm has an intrinsic
rate of 40 to 60 bpm and can be enhanced with atropine.
It has narrow QRS complexes because the impulse origi-
nates above the bifurcation of the bundle of His. An AV
junctional impulse is more effective than a ventricular
impulse because it is able to activate both ventricles si-
multaneously. Finally, AV junctional rhythm is more sta-
ble than a ventricular escape rhythm. A pacemaker may
be indicated if the AV block remains persistent and the
patient becomes symptomatic. A permanent pacemaker is
not needed and is a Class III indication if the AV block is
transient and is not expected to recur.
Infranodal: When the block is infranodal, a ventricular
escape rhythm usually comes to the rescue. The rhythm
has inherently slower rate of 20 to 40 bpm. Unlike AV
junctional rhythm, it cannot be enhanced with atropine.
Additionally, the QRS complexes are wide because both
ventricles are not activated synchronously. Thus, the ven-
tricles do not contract simultaneously, the beat is ineffec-
tive, and a lower cardiac output than a junctional escape
complex is generated. A ventricular rhythm, compared
with AV junctional rhythm, is not a stable rhythm. Finally,
an infranodal block is usually progressive and permanent
Figure 8.53: Complete Atrioventricular (AV) Dissociation from Ventricular Tachycardia. The rhythm
is ventricular tachycardia with complete AV dissociation. Note that the ventricular rate is faster than the atrial rate
(arrows), which should be the other way around in complete AV block.
Atrioventricular Block 109
and is frequently associated with structural abnormalities
not only of the conduction system, but also of the ventri-
cles. Before the era of pacemaker therapy, complete AV
block involving the distal conduction system was invari-
ably fatal. Insertion of a permanent pacemaker is cur-
rently the only effective therapy available.
The overall prognosis depends on the underlying cause of
the AV block. If the AV block is isolated and no structural
cardiac disease is present, the prognosis is similar to pa-
tients without AV block after a permanent pacemaker is
implanted.
Complete AV Dissociation
Complete AV dissociation: Complete AV dissocia-
tion and complete AV block are not necessarily the
same. Complete AV dissociation is a much broader
term than complete AV block and includes any ar-
rhythmia in which the atria and ventricles are com-
pletely independent from each other. Complete AV dis-
sociation includes complete AV block as well as other
arrhythmias not resulting from AV block such as ven-
tricular tachycardia (Fig. 8.53), junctional tachycardia
(Fig. 8.54), accelerated junctional rhythm (Fig. 8.55),
and accelerated ventricular rhythm (Fig. 8.56). In junc-
tional and ventricular tachycardia, the ventricular rate
is faster than the atrial rate. Thus, the atrial impulse
cannot conduct to the ventricles because the ventricles
do not have ample time to recover before the arrival of
the atrial impulse. In these examples, the dissociation
between atria and ventricles is not the result of AV
block.
Complete AV block: In complete AV block, the ven-
tricular rate is slower than the atrial rate. The ventricu-
lar rate is not only slower, but should be slow enough to
allow sufficient time for the ventricles to recover so that
it can be captured by the atrial impulse. Thus, the rate
of the ventricles should be 50 bpm, usually in the low
40s before AV block is considered complete.
Accelerated rhythms: In accelerated junctional or id-
ioventricular rhythm, the atria and ventricles may be
completely dissociated. The rate of the ventricles may
not be slow enough and may not be able to recover on
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110 Chapter 8

Figure 8.54: Complete Atrioventricular (AV) Dissociation from Junctional Tachycardia. The
rhythm is junctional tachycardia with a rate of 101 beats per minute. Both P waves and QRS complexes are regu-
lar but are completely dissociated. Although the P waves have no relation to the QRS complexes, complete AV
block is not present because the ventricular rate is not slow enough to be captured by the atrial impulse. The
arrows identify the P waves, which have no relation to the QRS complexes.

Figure 8.55: Complete Atrioventricular (AV) Dissociation from Accelerated Junctional Rhythm.
Lead II rhythm strip showing complete AV dissociation with an atrial rate of 100 beats per minute and a ventricular
rate at 80 beats per minute. The dissociation between the atria and ventricles may not be due to AV block. In com-
plete AV block, the ventricular rate should be in the 40s to allow enough time for the conduction system and the
ventricles to recover completely before the arrival of the next impulse. The P waves are marked by the arrows.

Figure 8.56: Complete Atrioventricular (AV) Dissociation from Accelerated Idioventricular

Rhythm. There is complete AV dissociation with an atrial rate of almost 100 beats per minute and ventricular rate
of 56 beats per minute. The QRS complexes are wide because of accelerated idioventricular rhythm. Although the
dissociation between the P waves and QRS complex may be due to complete AV block, this cannot be certain
because the ventricular rate is not slow enough. Thus, the rhythm is more appropriately complete AV dissociation
rather than complete AV block. The arrows identify the sinus P waves.

Figure 8.57: Complete Complete AV Dissociation

Atrioventricular (AV) Dissocia-
tion. Complete AV block is an exam-
ple of complete AV dissociation. The
other arrhythmias in which complete
Ventricular Accelerated
AV dissociation may occur are shown. idioventricular Junctional Junctional
tachycardia
Complete with complete rhythm with tachycardia rhythm with
AV block AV complete AV with complete complete AV
dissociation dissociation AV dissociation dissociation
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time before the arrival of the atrial impulse. This may
result in complete AV dissociation, not necessarily AV
block. Figure 8.57 shows the different arrhythmias that
can result in AV dissociation.
ECG Findings in Complete AV Dissociation
1. P waves and QRS complexes are completely dissociated and
have no relation to each other.
2. In complete AV dissociation, the underlying rhythm may be
ventricular tachycardia, junctional tachycardia, accelerated
junctional rhythm, accelerated ventricular rhythm, or com-
plete AV block.
Mechanism
Complete AV dissociation occurs when two completely inde-
pendent pacemakers, one controlling the atria and the other
controlling the ventricles, are present.
When there is ventricular tachycardia, junctional tachy-
cardia or accelerated junctional, or ventricular rhythms,
the sinus impulse may not be able to propagate to the ven-
tricles because the ventricular rate is faster than the atrial
rate. Absence of ventricular capture when the ventricular
rate is faster than the atrial rate is not necessarily because
of complete AV block, but may be from the ventricles be-
ing completely refractory every time atrial impulses arrive
at the ventricles. This is a form of electrical interference
resulting in AV dissociation. In these examples, complete
AV block is not present.
In complete AV block, there is complete absence of AV
conduction. The atrial impulse is unable to conduct
through the ventricles because of an abnormality in the
conduction system. The atrial impulse is given the oppor-
tunity to conduct to the ventricles, but is unable to do so
when complete AV block is present.
Clinical Implications
Complete AV dissociation is a broader term that includes any
rhythm where the atria and ventricles are completely inde-
pendent from each other and includes complete AV block as
well as other arrhythmias not resulting from complete AV
block such as ventricular tachycardia, junctional tachycardia,
AV junctional, or ventricular rhythm.
Complete AV block is just one of the many examples of
complete AV dissociation. For complete AV block to occur,
the ventricular rate should be slower than the atrial rate
and should be 50 bpm, usually in the low to mid-40s.
This will allow enough time for the ventricles to recover
before the next atrial impulse arrives. If the atrial impulse
cannot capture the ventricles even when the ventricular
Atrioventricular Block 111
rate is slow, then complete AV block is the cause of the AV
dissociation.
Treatment and Prognosis
Because there are other causes of complete AV dissociation
other than complete AV block, treatment and prognosis will
depend on the specific arrhythmia causing the AV dissociation.
Suggested Readings
2005 American Heart Association guidelines for cardiopul-
monary resuscitation and emergency cardiovascular care.
Part 7.3: management of symptomatic bradycardia and
tachycardia. Circulation. 2005;112:6777.
2005 American Heart Association guidelines for cardiopul-
monary resuscitation and emergency cardiovascular care.
Part 7.4: monitoring and medications. Circulation. 2005;
112:7883.
Barold SS, Hayes DL. Second-degree atrioventricular block: a
reappraisal. Mayo Clin Proc. 2001;76:4457.
Chatterjee K. Physical examination. In: Topol EJ, ed. Textbook of
Cardiovascular Medicine. 2nd ed. Philadelphia: Lippincott
Williams & Wilkins; 2002:280284.
Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE
2002 guideline update for implantation of cardiac pacemak-
ers and antiarrhythmia devices: summary article: a report of
the American College of Cardiology/American Heart Associ-
ation Task Force on Practice Guidelines (ACC/AHA/NASPE
Committee to update the 1998 pacemaker guidelines). Circu-
lation. 2002;106:21452161.
Epstein AE, DiMarco JP, Ellenbogen KA, et. al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a report of the American College of
Cardiology/American Heart Association Task Force on Prac-
tice Guidelines (Writing Committee to Revise the ACC/
AHA/NASPE 2002 Guideline Update for Implantation of
Cardiac Pacemakers and Antiarrhythmia Devices). Circula-
tion 2008;117:e350-e408.
Mangrum JM, DiMarco JP. The evaluation and management of
bradycardia. N Engl J Med. 2000;342:703709.
Marriot HJL. Intra-atrial, sino-atrial and atrio-ventricular
block. In: Practical Electrocardiography. 5th ed. Baltimore:
Williams & Wilkins; 1972:194211.
Marriott HJL, Menendez MM. A-V dissociation revisited. Prog
Cardiovas Dis. 1966;8:522538.
Narula OS, Scherlag BJ, Samet P, et al. Atrioventricular block.
Am J Med. 1971;50:146165.
Zipes DP, DiMarco JP, Gillette PC, et al. Guidelines for clinical in-
tracardiac electrophysiological and catheter ablation proce-
dures: a report of the American College of Cardiology/Ameri-
can Heart Association Task Force on Practice Guidelines
(Committee on Clinical Intracardiac Electrophysiologic and
Catheter Ablation Procedures), developed in collaboration
with the North American Society of Pacing and Electrophysiol-
ogy. J Am Coll Cardiol. 1995;26:555573.
LWBK271-C09_112-119.qxd 1/30/09 12:02 PM Page 112 Aptara Inc.
9
Intraventricular Conduction
Defect: Fascicular Block
Fascicular Block
Intraventricular conduction system: The intraven-
tricular conduction system includes the bundle of His,
the right and left bundle branches, the fascicular
branches of the left bundle branch, and the distal Purk-
inje fibers (Fig. 9.1).
Bundle of His: The bundle of His is a continuation
of the atrioventricular node. It is a short structure
that immediately divides into two branches: the
right and left bundle branches.
Right bundle: The right bundle branch follows the
right side of the ventricular septum and terminates
into a network of Purkinje fibers within the endo-
cardium of the right ventricle.
Left bundle: The left bundle branch immediately
fans into several branches, including a mid-septal
branch and two main fascicles: the left anterior and
left posterior fascicles.
n Left anterior fascicle: The left anterior fascicle
courses to the base of the anterior papillary mus-
cle before terminating into a network of Purkinje
fibers.
Atrioventricular node
Left bundle branch
His bundle
Left posterior fascicle
Right bundle Left anterior fascicle
branch
Purkinje fibers
Figure 9.1: The Intraventricular Conduction System.
The intraventricular conduction system consists of the bundle of
His, right and left bundle branches, the fascicular branches of
the left bundle branch, and the Purkinje fibers.
112
n Left posterior fascicle: The left posterior fasci-
cle terminates into a network of Purkinje fibers
after reaching the base of the posteromedial
papillary muscle.
Although the atria and ventricles are contiguous struc-
tures, the only pathway by which the sinus impulse can
reach the ventricles is through the atrioventricular node.
After exiting the atrioventricular node, conduction of
the impulse through the intraventricular conduction
system results in a fast and orderly sequence of ventricu-
lar activation. However, the sinus impulse can be patho-
logically delayed or interrupted anywhere within the in-
traventricular conduction system (Fig. 9.2).
Bundle branch block: If the sinus impulse is inter-
rupted within the bundle branches, the abnormality
is called bundle branch block.
n Right bundle branch block: If the impulse is
interrupted within the right bundle branch, the
conduction abnormality is called right bundle
branch block.
n Left bundle branch block: If the sinus impulse is
interrupted within the left bundle branch, the
conduction abnormality is called left bundle
branch block.
AV Node
Bundle of His
Left Bundle
Left posterior fascicle
Right Bundle
Left anterior fascicle
Figure 9.2: Diagrammatic Representation of the Atri-
oventricular Node and Intraventricular Conduction
System. The sinus impulse can propagate to the ventricles
only through the atrioventricular node and intraventricular con-
duction system, resulting in orderly sequence of ventricular acti-
vation.The sinus impulse can be blocked anywhere along this
conduction pathway, resulting in different types of intraventric-
ular conduction defect.
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Frontal Leads - Left Axis Deviation >-300
I aVR
aVL
II
Left Anterior III aVF
Fascicular Block
Precordial Leads - No Diagnostic Pattern
Fascicular block: If the sinus impulse is inter-
rupted within the fascicles, the conduction abnor-
mality is called fascicular block.
n Left anterior fascicular block: If the sinus im-
pulse is interrupted within the left anterior fasci-
cle, the conduction abnormality is called left an-
terior fascicular block (LAFB).
n Left posterior fascicular block: If the sinus im-
pulse is interrupted within the left posterior fas-
cicle, the conduction abnormality is called left
posterior fascicular block (LPFB).
Left Anterior Fascicular Block
Left anterior fascicular block: LAFB occurs when
the sinus impulse is delayed or interrupted within the
left anterior fascicle. LAFB is the most common intra-
ventricular conduction abnormality because the left
anterior fascicle is a long and thin structure that is
more delicate and more vulnerable to injury than the
rest of the conduction system.
Electrocardiogram findings: LAFB alters the elec-
trocardiogram (ECG) by abnormally shifting the axis
of the QRS complex to the left of 30. The most im-
portant leads in detecting the abnormal left axis devia-
tion are leads II and aVL.
Lead II: This is the most important lead in suspect-
ing that LAFB is present. In lead II, the QRS com-
plex is negative with an rS configuration (r wave is
smaller than the S wave). Leads III and aVF will also
show an rS pattern.
Lead aVL: A tall R wave in lead I (Rs complex) and
a qR pattern in aVL will confirm that the axis has
shifted to the left.
In LAFB, the right ventricle continues to be supplied by
the right bundle branch, and the left ventricle contin-
ues to be supplied by the left posterior fascicle. Therefore,
Intraventricular Conduction Defect: Fascicular Block 113
Figure 9.3: Left Anterior Fascicular Block.
The hallmark of LAFB is the presence of left axis de-
viation 30 with rS complexes in leads II, III, and
aVF and tall R waves in leads I and aVL. Briefly, LAFB
should always be suspected when there is negative
or rS complex in lead II with a tall R wave in lead I
(the essential leads are framed).
activation of both ventricles remains synchronous and
the duration of the QRS complex is not increased. It
normally remains at 0.08 to 0.10 seconds.
The ECG findings of LAFB are shown in Figures 9.3
and 9.4.
Common mistakes in left anterior fascicular block:
LAFB mistaken for anterior infarct: LAFB may
cause small q waves in V2 and in V3, which can be
mistaken for anteroseptal infarct (Fig. 9.5). These
microq waves may become more exaggerated if V1
and V2 are inadvertently positioned at a higher loca-
tion on the patients chest (at the 2nd rather than
the 4th intercostal space).
LAFB mistaken for inferior infarct: LAFB may be
confused with inferior myocardial infarction (MI)
because both can shift the QRS axis to the left of
30. However, inferior MI will show initial q waves
in leads II, III, and aVF (Fig. 9.6), whereas the QRS
complex in LAFB start with a small r wave in II, III,
and aVF (Fig. 9.5).
LAFB and inferior MI: LAFB and inferior MI may be
difficult to recognize when they occur together unless
the leads are recorded simultaneously (Fig. 9.7A).
LAFB: For LAFB to be present, (1) the axis of the
QRS complex should exceed 30, (2) both aVR and
aVL should end with R waves, and (3) the peak of
the R wave in aVL should occur earlier than the peak
of the R wave in aVR (Fig. 9.7B).
LAFB  inferior MI: When LAFB is associated with
inferior MI, a q wave in lead II should be present
(Fig. 9.8A) in addition to criteria 1, 2, and 3 for
LAFB listed previously (Fig. 9.8B).
ECG of LAFB
1. Frontal or limb leads:
Left axis deviation 30 (rS complexes in II, III, and aVF
and qR in I and aVL).
Normal QRS duration.
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114 Chapter 9

Figure 9.4: Left Anterior Fascicular Block. Twelve-lead electrocardiogram showing left anterior fascicular
block (LAFB).The axis of the QRS complex is 60. LAFB should always be suspected when a tall R wave is present in
lead I and deep S wave is present in lead II (the leads are framed). The QRS complexes remain normal in duration.
The precordial leads are not helpful in establishing the diagnosis, although poor R wave progression is usually pres-
ent. The changes in the precordial leads are due to extreme deviation of the electrical axis superiorly. These changes
may disappear if the leads are positioned two intercostal spaces higher than the standard location.

2. The horizontal or precordial leads are not needed for the di-
agnosis of LAFB.
Mechanism
The left anterior fascicle activates the anterior and superior
portions of the left ventricle. When there is LAFB, the area
supplied by the left anterior fascicle is the last to be activated.
This causes the axis of the QRS complex to shift superiorly
and to the left. The hallmark of LAFB is a shift in the QRS
axis to the left of 30. Although an axis of 45 is the tra-
ditional criteria used in the diagnosis of LAFB, a QRS axis
30 is accepted as LAFB.
The QRS complex is not widened when there is LAFB be-
cause the left ventricle has two overlapping sets of Purkinje
fibers: one from the left anterior fascicle and the other from
the left posterior fascicle. When there is LAFB, the left ventri-
cle is activated by the left posterior fascicle and the right ven-
tricle by the right bundle branch, thus both ventricles remain
synchronously activated. If there is any increased duration of

Figure 9.5: Left Anterior Fascicular Block. Left anterior fascicular block can cause small q waves in V2 and V3,
which can be mistaken for anterior myocardial infarction. These microq waves become more pronounced if leads
V1 to V3 are placed higher than the standard location and the patient is in a sitting position when the electrocardio-
gram is recorded.
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Figure 9.6: Inferior Myocardial Infarction. Left anterior fascicular block should not be confused with inferior my-
ocardial infarction (MI). In inferior MI, leads II, III, and aVF start with a q wave as shown here, rather than with a small r.

A B
Peak of the R wave
in aVR occurs later

Peak of the R
wave in aVL
occurs earlier

Figure 9.7: Left Anterior Fascicular Block. When leads aVR and aVL are simultaneously recorded (A), left an-
terior fascicular block is present when there is left axis deviation 30 and aVR and aVL both terminate with an R
wave. (B) Magnified to show that the peak of the R wave in aVL occurs earlier than the peak of the R wave in aVR.

A B

QS

Figure 9.8: Left Anterior Fascicular Block with Inferior MI. (A) Leads aVR and aVL are
recorded simultaneously and are magnified in (B). Note that the terminal R wave in aVR (arrow)
occurs later than the terminal R wave in aVL, consistent with left anterior fascicular block. In addi-
tion, q waves (QS) are present in lead II (A), consistent with inferior myocardial infarction.

115
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116 Chapter 9

Figure 9.9: Left Posterior Fascicular Block.
The most important feature of left posterior fascicu-
lar block (LPFB) is the presence of right axis devia-
tion 90. The diagnosis should be considered only
after chronic obstructive pulmonary disease and
other causes of right ventricular hypertrophy are
excluded. The presence of LPFB is suspected when
deep S wave is present in lead I (rS complex) and
tall R wave (Rs complex) is present in lead II (the
leads are framed).
Left posterior Fascicular Block
Frontal leads:
Axis: Right axis deviation >900. Other causes are excluded.
Lead I: rS complex
Lead aVF: Tall R in aVF and lead III with qR pattern
The duration of the QRS complex remains normal
Precordial leads: No diagnostic changes
Frontal Leads = Right Axis Deviation >900
I
aVR

aVL
II

Left Posterior
Fascicular Block aVF
III

Precordial Leads = No Diagnostic Pattern

the QRS complex, it will be minimal and should not exceed
0.01 to 0.02 seconds above baseline. Thus, the total duration
of the QRS complex will remain within 0.10 seconds unless
there is MI or left ventricular hypertrophy.
In LAFB, the left ventricle is initially activated by the left pos-
terior fascicle. Thus, the initial QRS vector is directed inferi-
orly and to the right, often causing q waves in V2 and V3. This
becomes exaggerated if the electrodes are positioned higher
on the chest or if the heart is oriented vertically.
rior papillary muscle. It courses subendocardially in the direc-
tion of the outflow tract of the left ventricle, and thus is subject
to higher intraventricular pressure than the rest of the conduc-
tion system. Because of its structure and location, LAFB is the
most common intraventricular conduction abnormality.
LAFB is a common cause of left axis deviation and should be
considered immediately when left axis deviation exceeds
30. LAFB may be difficult to recognize when combined
with inferior MI because both can cause left axis deviation.
LAFB: In LAFB, the QRS axis is 30 and leads II, III,

Clinical Significance and aVF start with small r waves. The terminal QRS vector
loop in the frontal plane is directed superiorly and left-
The left anterior fascicle is a long and thin structure that termi- ward in a counterclockwise direction. Thus, the peak of
nates into a network of Purkinje fibers at the base of the ante- the R in aVL occurs earlier than the peak of the R in aVR.

Figure 9.10: Normal Electrocardiogram. The QRS complexes are not widened, with normal axis of approxi-
mately 75.
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Figure 9.11: Left Posterior Fascicular Block. Twelve-lead electrocardiogram showing left posterior fascicu-
lar block (LPFB). The QRS complexes are not widened and the axis is shifted to 120. Before LPFB is diagnosed,
other causes of right axis deviation should first be excluded.
Inferior MI: In inferior MI, leads II, III, and aVF start
with q waves.
LAFB and inferior MI: There is LAFB if the QRS axis is
30, terminal R waves are present in aVR and aVL and
the peak of the R wave in aVL occurs earlier than the peak
of the R wave in aVR. If any q wave is present in lead II, in-
ferior MI is also present.
LAFB is commonly the result of hypertension, ischemic heart
disease, cardiomyopathy, aortic valve disease, and sclerosis or
fibrosis of the conduction system. Left ventricular hypertro-
phy is commonly associated with LAFB. Conversely, LAFB can
augment the tall R waves in aVL, which can mimic left ventric-
ular hypertrophy. In children, left axis deviation of 30 is
abnormal and is usually due to primum atrial septal defect.
Treatment and Prognosis
LAFB does not require any treatment. Therapy is directed to
the underlying cause of the LAFB.
The prognosis of LAFB depends on the underlying cause. If
this is the only conduction abnormality and no associated
cardiac disease is present, LAFB is generally benign.
Left Posterior Fascicular Block
Left posterior fascicular block: LPFB occurs when
conduction across the left posterior fascicle is delayed
or interrupted. It is the least common among all intra-
ventricular conduction abnormalities.
ECG Findings: The hallmark of LPFB is a shift in the
electrical axis of the QRS complex to the right of 90
Intraventricular Conduction Defect: Fascicular Block 117
(Fig. 9.9). Because LPFB is uncommon, other more
common causes of right axis deviation should first be
excluded before LPFB is diagnosed. The QRS com-
plexes are not widened because the left ventricle con-
tinues to be activated by the left anterior fascicle. A
normal ECG is shown in Fig. 9.10. For comparison, the
ECG of LPFB is shown in Fig. 9.11.
Common mistakes in LPFB:
Right ventricular hypertrophy mistaken for
LPFB: LPFB is relatively uncommon and is consid-
ered a diagnosis of exclusion. Other causes of right
axis deviation, such as right ventricular hypertrophy
or pulmonary disease, should first be excluded before
the diagnosis of LPFB is considered (Figs. 9.12 and
9.13). This contrasts with LAFB, where the diagnosis
is considered immediately when the axis is 30.
Lateral MI mistaken for LPFB: High lateral MI can
cause right axis deviation 90 and can be mistaken
for LPFB. In LPFB, rS complexes are present in I and
aVL (Fig. 9.11). In lateral MI, QS complexes are
present in these leads (Fig. 9.14).
ECG of LPFB
1. Frontal or limb leads:
Right axis deviation 90 with negative or rS complex in
I and aVL and qR in III and aVF.
The QRS complexes are not widened.
Other causes of right axis deviation have been excluded.
2. Horizontal or precordial leads:
The precordial leads are not necessary in the diagnosis of
LPFB.
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Figure 9.12: Right Ventricular Hypertrophy. The frontal leads show all features of left posterior fascicular
block (LPFB). However, tall R waves are present in V1, suggesting right ventricular hypertrophy and not LPFB.

Figure 9.13: Right Ventricular Hypertrophy. There is right atrial enlargement with peaked P waves in leads
II, III, and aVF (arrows). There is clockwise rotation of the QRS complexes in the precordial leads. This
electrocardiogram is consistent with right ventricular hypertrophy and not left posterior fascicular block.

Figure 9.14: Lateral Myocardial Infarction. Lateral myocardial infarction (MI) with QS complexes in I and aVL
can be mistaken for left posterior fascicular block (LPFB) as shown here. In LPFB, leads I and aVL have rS complexes,
whereas in lateral MI, these leads start with q waves. Q waves are also present in V1 to V4 because of anterior MI.

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Mechanism
The left posterior fascicle activates the posteroinferior left
ventricular free wall, which is to the right and inferior to that
activated by the left anterior fascicle. This portion of the left
ventricle is the last to be activated when there is LPFB, thus
causing the axis of the QRS complex to shift inferiorly and to
the right. While a QRS axis 100 is traditionally used to
identify LPFB, a QRS axis 90 is generally accepted as
LPFB.
The QRS complex is not widened when there is LPFB because
the left ventricle continues to be activated by the left anterior
fascicle and the right ventricle by the right bundle branch, re-
sulting in synchronous activation of both ventricles.
Clinical Significance
LPFB is a diagnosis of exclusion since LPFB is relatively un-
common. This contrasts with LAFB, in which the diagnosis is
considered outright when there is left axis deviation 30.
Before the diagnosis of LPFB is considered, other, more com-
mon, causes of right axis deviation such as pulmonary dis-
ease and other causes of right ventricular hypertrophy
should first be excluded.
In contrast to the left anterior fascicle, the left posterior fasci-
cle has a dual blood supply, originating from the septal per-
forating branches of the left anterior descending coronary
artery anteriorly and from the septal perforating branches of
the posterior descending artery posteriorly. It is short, thick,
and broad and courses along the inflow tract of the left ven-
tricle before terminating into a network of Purkinje fibers at
the base of the posteromedial papillary muscle. It is therefore
protected and subjected to less intraventricular pressure
compared with the left anterior fascicle. Because of its struc-
ture, location, and blood supply, LPFB is the least common
among all intraventricular conduction abnormalities.
The most important lead in recognizing LPFB is lead I. This
will show a negative or rS complex, with the S wave deeper
than the size of the r wave. This is accompanied by tall R
waves in leads aVF and III.
Right axis deviation due to high lateral MI can be mistaken
for LPFB. Correspondingly, LPFB can obscure the ECG
changes of inferior MI.
Intraventricular Conduction Defect: Fascicular Block 119
The causes of LPFB are the same as that of LAFB and include
coronary disease, hypertension, cardiomyopathy, acute my-
ocarditis, valvular disease (especially aortic stenosis), and de-
generative diseases of the conduction system.
Treatment
Treatment is directed toward the underlying cause of the LPFB.
Prognosis
Because the left posterior fascicle is the least vulnerable and
the last to be involved when there is intraventricular conduc-
tion defect, LPFB seldom occurs independently and is fre-
quently seen in combination with right bundle branch block
or with LAFB. LPFB, therefore, indicates a more significant
and more advanced form of conduction abnormality than
LAFB. LPFB in combination with LAFB can result in left
bundle branch block. The prognosis depends on the cause of
the conduction abnormality.
Suggested Readings
Dunn MI, Lipman BS. Abnormalities of ventricular conduction:
fascicular block, infarction block, and parietal block. In:
Lippman-Massie Clinical Electrocardiography. 8th ed. Chicago:
Yearbook Medical Publishers, Inc.; 1989:148159.
Elizari MV, Acunzo RS, Ferreiro M. Hemiblocks revisited. Circu-
lation. 2007;115:11541163.
Marriott HJL. The hemiblocks and trifascicular block. In: Practical
Electrocardiography. 5th ed. Baltimore: The Williams and
Wilkins Company; 1972:8694.
Sgarbossa EB, Wagner GS. Electrocardiography: In: Topol EJ, ed.
Textbook of Cardiovascular Medicine. 2nd ed. Philadelphia:
Lippincott Williams & Wilkins; 2002:13301354.
Warner RA, Hill NE, Mookherjee S, et al. Electrocardiographic
criteria for the diagnosis of combined inferior MI and left
anterior hemiblock. Am J Cardiol. 1983;51:718722.
Warner RA, Hill NE, Mookherjee S, et al. Improved electrocar-
diographic criteria for the diagnosis of left anterior hemi-
block. Am J Cardiol. 1983;51:723726.
Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for
intraventricular conduction disturbances and pre-excitation.
J Am Coll Cardiol. 1985;5:12611275.
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10
Intraventricular Conduction
Defect: Bundle Branch Block
Right Bundle Branch Block
Right bundle branch block: Conduction of the sinus
impulse can be interrupted at the level of the right
bundle branch resulting in right bundle branch block
(RBBB) (Fig. 10.1).
ECG findings: Unlike fascicular blocks in which the
electrocardiogram (ECG) findings are best seen in the
frontal leads, the ECG changes of RBBB are best recog-
nized in the precordial leads V1 and V6. The hallmark of
RBBB is the presence of wide QRS complexes measur-
ing 0.12 seconds with large terminal R waves in V1
and wide terminal S waves in V6 as well as in leads I and
aVL. The septal Q waves are preserved.
Bundle branch block is a more extensive conduction
abnormality than the fascicular blocks. In RBBB, the
QRS complex is widened by 0.12 seconds because ac-
tivation of the entire right ventricle is delayed.
The axis of the QRS complex is not significantly
changed and remains normal when there is RBBB (Fig.
10.2, Fig. 10.3). The axis may shift to the left if left an-
terior fascicular block (LAFB) is present or to the right
if left posterior fascicular block (LPFB), pulmonary hy-
pertension, or right ventricular hypertrophy is present.
In the setting of RBBB, only the first 0.06 to 0.08 sec-
onds of the QRS complex should be used in calculating
the axis of the QRS complex because the terminal por-
tion of the QRS complex represents delayed activation
of the right ventricle (Fig. 10.3).

Figure 10.1:Right Bundle Right Bundle Branch Block

Branch Block. In right bundle
branch block, the QRS complexes
are wide measuring 0.12 seconds.
Large terminal R waves are present
in V1 with rR or rsR configuration.
V6 shows wide S wave with a qRS or
RS configuration. The onset of the
intrinsicoid deflection also called R
peak time is prolonged in V1 but
normal in V6.
Wide QRS complexes measuring 0.12 second.
V1:
Large terminal R waves with rR or rsR configuration.
Onset of intrinsicoid deflection (R peak time) >0.05 sec.
V6 and leads on left side of ventricular septum (I and aVL):
Wide terminal S waves are present.
Septal q waves are preserved.
Onset of intrinsicoid deflection (R peak time) is delayed in V1 (>0.05 sec)

V1 Terminal
R wave

rR RR rsR

Onset of intrinsicoid deflection (R peak time) is normal in V6 (0.05 sec)

Right Bundle V6
Branch Block
Wide terminal
qRS S wave RS

120
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Intraventricular Conduction Defect: Bundle Branch Block 121

Figure 10.2: Complete Right Bundle Branch Block. The QRS complexes are wide measuring 0.12
seconds. rsR configuration is present in V1 and qRs configuration is present in V6. Wide S waves are present in leads I
and V6. The axis of the QRS complex in the frontal plane is normal.

ECG findings: The typical features of RBBB are seen in

RBBB  LAFB
Right bundle branch block  left anterior fascicu-
lar block: RBBB can occur in combination with a fas-
cicular block. Thus, RBBB  LAFB are present if the si-
nus impulse is simultaneously interrupted at the right
bundle branch and left anterior fascicular branch.
RBBB in combination with LAFB is an example of a bi-
fascicular block because two conduction pathways are
interrupted. Activation of the ventricles can occur only
through the remaining left posterior fascicle.
the precordial leads and that of LAFB in the frontal
leads (Fig. 10.4).
RBBB: The QRS complexes are wide measuring
0.12 seconds because of the presence of RBBB.
The characteristic rR or rsR pattern is present in
V1, and wide S waves are present in V6.
LAFB: In the frontal plane, the axis of the QRS com-
plex is 30 with rS in lead II and tall R wave in
aVL.
RBBB  LPFB: RBBB  LPFB can occur when conduc-
tion across the right bundle and left posterior fascicle is

Figure 10.3: Right Bundle Branch Block Alternating with Normal Conduction. Note that when right
bundle branch block occurs (arrows), the axis of the QRS complex using only the first 0.06 to 0.08 seconds is not sig-
nificantly changed when compared with the normally conducted QRS complexes.
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122 Chapter 10

Figure 10.4: Diagrammatic Representation of RBBB + LAFB

Right Bundle Branch Block  Left Anterior Fas-
cicular Block. The QRS complexes are wide. The pre-
cordial leads show classical RBBB with rR, RR, or rsR in
V1 and qRS in V6. The limb leads show left axis deviation
30 with deep rS complex in lead II and tall R in aVL.
The QRS complexes measure 0.12 second due to RBBB
Precordial leads: RBBB in V1 and in V6
Frontal leads: LAFB with left axis deviation >-300
Precordial leads = classical RBBB
V1 V6

rR RR rsR

Frontal leads = Left axis deviation >-300

RBBB + LAFB

Lead II aVL

simultaneously interrupted. RBBB  LPFB is also an
example of bifascicular block (Fig. 10.5, Fig. 10.6, Fig.
10.7, Fig. 10.8).
ECG findings: The presence of RBBB and LPFB is rec-
ognized separately.
RBBB: The typical features of RBBB are best recog-
nized in the precordial leads as widening of the QRS
complex (0.12 seconds) with a characteristic large
terminal R (rR or rsR) in V1 and wide S in V6.
LPFB: LPFB is best recognized in the frontal plane as
a shift in the QRS axis 90. Deep S waves are pres-
ent in lead I, with tall R waves in leads III and aVF.
For LPFB to be considered, other causes of right axis
deviation should first be excluded.

Figure 10.5: Diagrammatic Rep- RBBB + LPFB

resentation of Right Bundle
Branch Block  Left Posterior Wide QRS complexes measuring 0.12 seconds due to RBBB
Fascicular Block. The classical pat- Precordial leads: RBBB in V1 and in V6
tern of right bundle branch block is rec-
Frontal leads: LPFB with right axis deviation >900
ognized in the precordial leads with rR
or rsR in V1 and qRS in V6. The limb
leads show right axis deviation 90
with rS in lead I and tall R wave in lead
aVF from left posterior fascicular block. Precordial Leads = Classical RBBB
V1 V6

Frontal Leads = Right Axis Deviation > 900

RBBB + LPFB

Lead aVF
Lead I

RBBB and Fascicular Block

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Figure 10.6: Uncomplicated Right Bundle Branch Block. The QRS complexes are wide measuring 0.12
seconds with rsr configuration in V1 and qRs configuration in V6. Wide S waves are noted in leads I and V6.The axis of
the QRS complex in the frontal plane is normal.

Figure 10.7: Right Bundle Branch Block  Left Anterior Fascicular Block. Right bundle branch block is
recognized by the presence of wide QRS complexes measuring 0.12 seconds with rR or rsR in V1 and wide S waves
in V6. Left anterior fascicular block is diagnosed by the presence of left axis deviation of 60 in the frontal leads.

Figure 10.8: Right Bundle Branch Block  Left Posterior Fascicular Block. There is right bundle
branch block with rR pattern in V1 and RS in V6. Left posterior fascicular block is diagnosed by the presence of right
axis deviation of 120 in the frontal plane.

123
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124 Chapter 10

ST and T Wave Changes in Right

Figure 10.9: A: Uncomplicated RBBB
V1 V6
Bundle Branch Block. (A) When uncomplicated
right bundle branch block is present, the terminal por-
tion of the QRS complex and the ST segment and T
waves are discordant. Note that the small arrows
(pointing to the terminal QRS complex) are opposite in Discordant T waves
direction to the large arrows, which is pointing to the B: RBBB + Myocardial Abnormality
direction of the T wave. (B) When the ST and T waves V1 V6
are concordant (arrows are pointing in the same direc-
tion), the ST and T wave changes are primary and indi-
cate the presence of a myocardial abnormality.
Concordant T waves

Primary repolarization changes: When the ST and T

RBBB: Concordant and
Discordant T Waves
Secondary repolarization changes: In uncompli-
cated RBBB, the ST segment and T wave are normally
discordant and opposite in direction to the terminal
portion of the QRS complex (Fig. 10.9A). These ST-T
changes are secondary to the abnormal activation of the
ventricles. They are not included as criteria in the diag-
nosis of RBBB.
V1: Because the terminal portion of the QRS com-
plex is an R wave in V1 (which is upright), the ST
segment is isoelectric or depressed and the T wave is
normally inverted (Fig. 10.9A).
V6: Because the terminal portion of the QRS com-
plex is an S wave in V6, the ST segment is isoelectric
or elevated and the T wave is normally upright.
waves are concordant (in the same direction as the ter-
minal portion of the QRS complex; Fig. 10.9B), in the
setting of RBBB, these changes are primary and due to
the presence of an intrinsic myocardial disorder such as
cardiomyopathy or myocardial ischemia rather than
secondary to the abnormal activation of the ventricles.
Incomplete RBBB
Incomplete RBBB: Incomplete RBBB has all the fea-
tures of complete RBBB except that the duration of the
QRS complex is 0.12 seconds. In incomplete RBBB,
there is delay rather than complete interruption of the
impulse to the right ventricle.
ECG Findings: The ECG findings of incomplete
RBBB are identical to those of complete RBBB except

Figure 10.10: Incomplete Right Bundle Branch Block. The QRS complexes are only minimally widened,
measuring 0.12 seconds, with rSr in V1 and a minimally wide S wave in leads I and V6. This electrocardiogram is
otherwise similar to that of complete right bundle branch block, as shown in Figure 10.6.
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Intraventricular Conduction Defect: Bundle Branch Block
Figure 10.11: Intermittent Right Bundle Branch Block. Lead V1 rhythm strip showing
intermittent right bundle branch block (RBBB). Note the change in the width and configuration
of the QRS complex in V1 with the onset of RBBB.
that the QRS complexes measure 0.12 seconds
(Fig. 10.10). The axis of the QRS complex is normal
unless there is LAFB or LPFB.
n V1: Right precordial lead V1 shows an rsr or rR
pattern very similar to that of complete RBBB.
n V6: Left precordial lead V6 will show a slightly
widened S wave.
Intermittent RBBB: RBBB often occurs intermittently
before it becomes fixed (Fig. 10.11). Intermittent RBBB
is usually rate related meaning that it usually occurs
when the heart rate exceeds a certain level.
Common Errors in RBBB
Ectopic ventricular impulses: Ectopic impulses origi-
nating from the ventricles have wide QRS complexes.
These ectopic impulses are wide because they do not fol-
low the normal conduction system and spread to the ven-
tricles by muscle cell to muscle cell conduction. The wide
complexes may be mistaken for bundle branch block.
Ventricular tachycardia: A common example is
ventricular tachycardia with RBBB configuration.
Although the QRS complexes are wide with tall R
waves in V1, it is erroneous to conclude that there is
RBBB during ventricular tachycardia. The ventricu-
lar tachycardia may originate from the left ventricle
and spread to the right ventricle, causing the QRS
complexes to have a RBBB pattern. Despite this ap-
pearance, RBBB is not present.
Accelerated idioventricular rhythm (AIVR):
When ventricular impulses resulting from acceler-
ated idioventricular rhythm occur, the wide QRS
complexes may have a RBBB pattern and may be
mistaken for RBBB (Fig. 10.12).
In true RBBB, the impulse should be sinus or
supraventricular. When the impulse originates from
the ventricles or below the bifurcation of the bundle of
His, the impulse is ventricular. A ventricular impulse
125
may demonstrate an RBBB configuration, even though
RBBB is not present.
ECG Findings in RBBB
1. Wide QRS complexes measuring 0.12 seconds.
Right-sided precordial leads V1.
n Large terminal R waves with rSR or rR often in an
M-shaped configuration.
n Onset of intrinsicoid deflection or R peak time is pro-
longed and is 0.05 seconds.
Left-sided precordial leads V6.
n Wide S wave with qRS, RS, or rS pattern.
n Septal Q waves are preserved.
n Onset of intrinsicoid deflection or R peak time is nor-
mal and is 0.05 seconds.
Frontal or limb leads:
n Wide S waves in leads I and aVL.
n The axis of the QRS complex is normal.
2. ST segment and T wave are opposite in direction (normally
discordant) to the terminal QRS complex. These ST and T
wave changes are not included as criteria for the diagnosis of
RBBB.
Right-sided precordial leads V1 or V2:
n ST segment isoelectric or depressed.
n T wave inverted.
Left sided precordial leads V5 or V6:
n ST segment isoelectric or elevated.
n T wave is upright.
Mechanism of RBBB
Wide QRS complex: The intraventricular conduction sys-
tem activates both ventricles synchronously, resulting in a
narrow QRS complex. When RBBB occurs, conduction of
the impulse through the right bundle branch is delayed or in-
terrupted, whereas conduction to the left bundle branch and
left ventricle is preserved. Activation of the right ventricle is
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126 Chapter 10

Figure 10.12: Accelerated Idioventricular Rhythm. The rhythm is normal sinus as shown by the first
two complexes on the left. The wide QRS complexes that follow (arrows) look like intermittent right bundle
branch block with tall R waves in V1. The wide QRS complexes are ventricular escape complexes because of
accelerated idioventricular rhythm. Note that the wide QRS complexes are not preceded by P waves and occur
only when there is slowing of the sinus node.

abnormal because the impulse must originate from the left
ventricle by muscle cell to muscle cell conduction. Because the
ventricles are activated sequentially instead of synchronously,
the QRS complexes are wide measuring 0.12 seconds. The
wide QRS complex can be divided into two halves: the initial
half representing left ventricular activation and the terminal
half representing right ventricular activation.
Vector 1: In RBBB, vector 1 or septal activation is not al-
tered, thus the initial portion of the QRS complex re-
mains preserved. A small r wave is normally recorded in
lead V1, and a normal septal q wave is recorded in V6 as
well as in leads located on the left side of the ventricular
septum (leads I and aVL).
Vector 2: Activation of the left ventricular free wall or
vector 2 is also preserved and normally occurs from en-
docardium to epicardium in a right to left direction. This
result in deep S waves in V1 and tall R waves in V6. Activa-
tion of the right side of the septum, however, is no longer
possible because the right bundle branch is blocked.
Thus, septal activation continues unopposed in a left to
right direction, which is opposite the direction of activa-
tion of the left ventricular free wall. Because the septum
and left ventricular free wall are activated in opposite di-
rections, the depth of the S wave in V1 and the height of
the R wave in V6 are smaller than normal.
Vector 3: Whenever there is an intraventricular conduc-
tion abnormality, the area with the conduction abnor-
mality is always the last to be activated. Activation of the
right ventricle, therefore, is the last to occur in RBBB (vec-
tor 3). Because the right bundle branch supplies the right
ventricle, and the right ventricle is located anterior and to
the right of the left ventricle, the terminal impulse will be
directed to the right and anteriorly. This results in a large
terminal R in V1 and wide terminal S in V6 (and also in
leads I and aVL). This is the most distinctive abnormality
of RBBB. This terminal impulse is slow because it is con-
ducted by direct myocardial spread and is unopposed be-
cause activation of the right ventricle is still ongoing,
whereas activation of the rest of the ventricle is already
completed.
Delayed onset of the intrinsicoid deflection or R peak
time: The ventricular activation time is the time from onset
of the ventricular impulse to the arrival of the impulse at the
recording precordial electrode. It is measured from the onset
of the QRS complex to the height of the R or R wave. The
turning point or abrupt downward deflection of the R or R
wave toward baseline is called the intrinsicoid deflection (see
Chapter 6, Depolarization and Repolarization). For practi-
cal purposes, the R peak time has been recommended by
the Cardiology Task Force of the World Health Organiza-
tion/International Society and Federation to represent the on-
set of the intrinsicoid deflection. The normal onset of the in-
trinsicoid deflection in V1 is 0.03 seconds. When there is
RBBB, the onset of the intrinsicoid deflection in V1 is pro-
longed and measures 0.05 seconds because conduction of the
impulse across the right ventricle is delayed. The onset of the
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Intraventricular Conduction Defect: Bundle Branch Block
intrinsicoid deflection in leads V5 or V6 is preserved (normal
0.05 seconds) because the left bundle branch is intact.
Abnormal ST-T changes: The ST and T abnormalities in
RBBB are secondary to abnormal activation of the ventricles
and are normally discordant to the terminal portion of the
QRS complex. The ST-T changes are not considered criteria
for the diagnosis of RBBB.
QRS Axis: In uncomplicated RBBB, the axis of the QRS
complex is within normal limits. However, when RBBB oc-
curs in association with pulmonary hypertension or condi-
tions that can cause right ventricular hypertrophy, the axis of
the QRS complex may shift to the right. The axis of the QRS
complex can also become abnormal when there is fascicular
block or previous myocardial infarct.
Clinical Significance
Incomplete RBBB with a terminal r wave in V1 or V2 does
not always imply that a conduction block is present in the
right bundle branch. This ECG pattern could also be due to
delayed conduction of the impulse to the right ventricle,
causing the right ventricle to be partly activated by the left
bundle branch. It could also be due to delayed activation of
the base of the right or left ventricle due to a focal area of hy-
pertrophy. For example, in infants and children, the terminal
r in V1 may be due to hypertrophy of the outflow tract of the
right ventricle, a condition that may persist through adult-
hood. It has also been shown than an rSr pattern in V1 or V2
may occur if the precordial leads V1 and V2 are inadvertently
positioned higher than the correct location at the 4th inter-
costal space, a common error among house officers or tech-
nicians who are not properly trained to record ECGs.
Because the right bundle branch is partially subendocardial in
location, it is vulnerable to sudden and severe increases in right
ventricular pressure. RBBB can therefore occur in the setting
of pulmonary hypertension or acute pulmonary embolism.
The right bundle branch is also vulnerable to local injury dur-
ing right heart catheterization. Thus, extreme caution should
be exercised when inserting a pulmonary artery catheter in a
patient who has preexistent left bundle branch block (LBBB).
RBBB may initially occur intermittently before it becomes
fixed. When RBBB is intermittent, it is usually rate related. In
rate-related bundle branch block, bundle branch block oc-
curs only when the heart rate increases above a certain
threshold. Normal conduction is restored when the heart
rate slows down to baseline. The presence of rate-related
bundle branch block is often suspected when the wide QRS
complexes normalize after a long compensatory pause of a
premature ectopic impulse.
Clinical significance: RBBB can occur as an isolated finding
in the general population, including young individuals without
evidence of cardiac disease. Among 110,000 subjects screened
for cardiovascular disease during a 25-year period, isolated
RBBB (no evidence of heart disease or hypertension) occurred
in 198 cases (0.18%) and was associated with an excellent prog-
nosis. In another study consisting of 1,142 elderly men fol-
127
lowed in the Baltimore Longitudinal Study on Aging, 39 or
3.4% had complete RBBB. Twenty-four of these patients had
no evidence of heart disease. Long-term follow-up of patients
who are apparently healthy and completely asymptomatic had
not shown any adverse effects on mortality and morbidity.
RBBB and LAFB is a common combination because the right
bundle and left anterior fascicle are adjacent to each other,
straddling both sides of the ventricular septum. Both are sup-
plied by the left anterior descending coronary artery. Thus, a
concurrent RBBB and LAFB is a common complication of
acute anteroseptal myocardial infarction (MI). When RBBB
with fascicular block is due to acute anterior MI, the myocardial
damage is usually extensive, resulting in a higher incidence of
atrioventricular (AV) block, pump failure, and ventricular
arrhythmias. However, if the RBBB is due to degenerative dis-
ease of the conduction system with preservation of myocardial
function, progression to complete AV block is slow, and long-
term prognosis is good.
RBBB and MI: The presence of RBBB generally does not
conceal the ECG changes associated with Q wave MI. This
contrasts with LBBB, where ECG changes of acute MI are
usually masked by the conduction abnormality. Thus, Q
waves will continue to be useful in signifying acute or remote
MI in patients with RBBB.
RBBB and stress testing: According to the American College
of Cardiology/American Heart Association guidelines for
chronic stable angina, the presence of RBBB on a baseline ECG
during exercise stress testing will not interfere with the detection
of myocardial ischemia. The ST segment depression in leads V1
to V3 may not be related to myocardial ischemia; however, ST
depression in leads V5, V6, II, and aVF is as reliable in indicating
myocardial ischemia as in ECGs without RBBB. Thus, patients
with RBBB on baseline ECG may undergo ECG exercise stress
testing similar to patients without the conduction abnormality.
This contrasts with patients with LBBB in whom ST depression
does not necessarily imply the presence of myocardial ischemia
(see Left Bundle Branch Block section in this chapter). Unlike
patients with RBBB, patients with LBBB should undergo imag-
ing in conjunction with ECG stress testing.
RBBB and congestive heart failure: In patients with se-
vere left ventricular dysfunction with ongoing symptoms of
congestive heart failure intractable to standard medical ther-
apy, the presence of wide QRS complexesincluding patients
with RBBBmay be candidates for resynchronization ther-
apy (see Left Bundle Branch Block section in this chapter).
Causes of RBBB: RBBB can be due to several causes, includ-
ing acute MI, cardiomyopathy, pulmonary hypertension, pul-
monary embolism, cor pulmonale, acute myocarditis, valvular
heart disease (especially aortic stenosis), sclerodegenerative
changes involving the conduction system, infiltrative diseases
such as sarcoidosis and amyloidosis, Chagas disease, and con-
genital heart disease such as tetralogy of Fallot and Ebsteins
anomaly. It may occur as a complication of cardiac surgery or
interventional procedures such as cardiac catheterization,
percutaneous coronary intervention, radiofrequency ablation,
or alcohol ablation of the ventricular septum in patients with
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128 Chapter 10

idiopathic hypertrophic subaortic stenosis. It may also be a
normal finding in young individuals.
Auscultatory findings: Auscultatory findings associated
with RBBB include delayed closure of the pulmonic valve re-
sulting in wide splitting of the second heart sound. There
may also be delay in the closure of the tricuspid valve result-
ing in wide splitting of the first heart sound.
Left Bundle Branch Block
Treatment and Prognosis
The overall prognosis of patients with RBBB depends on the
associated cardiac abnormality.
Asymptomatic RBBB does not require any therapy and may
be a normal finding in younger asymptomatic individuals
or in older patients without evidence of cardiac disease.
When RBBB is an isolated abnormality, progression to com-
plete AV block is uncommon, occurring 1% per year. Even
patients with isolated RBBB who subsequently go on to de-
velop complete AV block can expect to have a normal life
span after placement of a permanent pacemaker.
RBBB with or without fascicular block complicating
acute anterior MI is associated with a mortality of 20%.
Most of these patients have extensive myocardial damage
and will succumb to ventricular arrhythmias and pump
failure rather than complete AV block. Thus, insertion of
a permanent pacemaker in these patients may prevent AV
block, but may not alter the overall prognosis. Practice
guidelines recommend that patients who survive an acute
MI with a final ejection fraction 35% should have an
automatic defibrillator implanted regardless of the pres-
ence or absence of arrhythmias or conduction abnormal-
ity. The underlying cardiac disease, therefore, is most im-
portant in defining the prognosis of patients with RBBB.
LBBB: Conduction of the sinus impulse can be inter-
rupted at the main left bundle or more distally at the
level of both fascicles resulting in LBBB (Fig. 10.13).
ECG findings: When the left bundle branch is blocked,
activation of the left ventricle is delayed resulting in wide
QRS complexes that measure 0.12 seconds. The ECG
findings of LBBB are best recognized in precordial leads
V1 and V6. In lead V1, a QS or rS complex is recorded.
In V6, the septal q wave is no longer present. A tall
monophasic R wave often with initial slurring or M-
shaped configuration is present, and onset of intrinsicoid
deflection or R peak time is prolonged (0.05 seconds).
Incomplete LBBB: Incomplete LBBB is similar to
complete LBBB except that the duration of the QRS
complex is 0.12 seconds. In incomplete LBBB,
there is a delay (rather than a complete interruption)
in the conduction of the impulse to the left bundle
branch.

Figure 10.13: Left Bundle Left Bundle Branch Block

Branch Block. V1 and V6 are
the most important leads in rec- Wide QRS complexes measuring 0.12 second
ognizing left bundle branch
V1:
block. The QRS complexes in V1
QS or rS complexes
will show deep QS or rS
complexes and V6 will show rR, V6 and leads on left side of ventricular septum (I and aVL):
monophasic R, or RR often M- Septal q waves are absent
shaped configuration. The R Monophasic R, RR, slurred R or M-shaped R
peak time or onset of the intrin- Onset of intrinsicoid deflection or R peak time is prolonged
sicoid deflection in V6 is shown (>0.05 sec)
by the arrows and is delayed
V1 Onset of intrinsicoid deflection (R peak time) is normal in V1
(0.05 seconds). No septal Q
waves are present.

rS QS QS

R peak time is prolonged in V6 measuring >0.05 second

V6

Left Bundle RR R RR
Branch Block
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Intraventricular Conduction Defect: Bundle Branch Block 129

Figure 10.14: Left Bundle Branch Block. In left bundle branch block, the QRS complexes are wide with a QS
or rS complex in V1 and tall monophasic R wave in V6 without septal q waves. The ST segment and T waves are nor-
mally discordant.

ECG Findings: In incomplete LBBB, the QRS complexes
are slightly widened, measuring 0.12 seconds. All the
features of LBBB are present; septal q waves in V5 or V6
are absent, and either a QS complex or a small r wave
(rS complex) is present in V1 (Fig. 10.14, Fig. 10.15).
The left ventricle is supplied by two main fascicles: the
left anterior and left posterior fascicles. LBBB is there-
fore considered a bifascicular block. Although a mid-
septal fascicle also exists, its significance is uncertain
and there are presently no diagnostic criteria for lesions
involving the mid-septal branch.
In LBBB, the abnormal activation of the left ventricle can
result in ECG abnormalities that may be mistaken for left
ventricular hypertrophy. The presence of abnormal q
waves and ST-T abnormalities can mimic MI. Con-
versely, LBBB can mask the ECG changes of acute MI.
The abnormal activation of the left ventricle can cause
wall motion abnormalities, even in patients without my-
ocardial disease. It may also result in mitral regurgitation
because of asynchrony in the contraction of the anterior
and posterior papillary muscles. These abnormalities are
enhanced when myocardial disease is superimposed on

Figure 10.15: Incomplete Left Bundle Branch Block. In incomplete left bundle branch block (LBBB), the
QRS complexes have all the features of LBBB. QS or rS configuration is present in V1, tall monophasic R waves are
present in V6, and no septal q waves in V6. The duration of the QRS complex, however, is 0.12 seconds.
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130 Chapter 10

Figure 10.16: Left Bundle Branch Block with Unusually Wide QRS Complexes. The QRS complexes
measure almost 0.20 seconds and the axis is shifted to the left. The unusual width of the QRS complexes is often a
marker of severe myocardial disease, especially when there is right or left axis deviation.

the conduction defect. In general, patients with LBBB
with very wide QRS complexes (Fig. 10.16) have more
severe contraction abnormalities and lower ejection
fractions compared with patients with LBBB with nar-
rower complexes.
The axis of the QRS complex in LBBB is variable. When
LBBB is associated with left axis deviation, the conduc-
tion abnormality is more widespread and may involve
the distal fascicles and Purkinje system. When right
axis deviation is present, it may be associated with dif-
fuse myocardial disease and biventricular enlargement.
Secondary ST and T wave changes: Similar to
RBBB, the ST-T changes are not included as criteria in
the ECG diagnosis of LBBB. The ST-T changes associ-
ated with uncomplicated LBBB are secondary to abnor-
mal activation of the left ventricle. The direction of the
ST segment and T wave is normally discordant or op-
posite that of the QRS complex (Fig. 10.17A).
V1: In V1, the ST segment is normally elevated and
the T wave upright because the terminal portion of
the QRS complex is an S wave, which is negative or
downward.

A. Uncomplicated LBBB B. LBBB + Myocardial abnormality

Discordant T waves Concordant T waves

V1, V2 or V3 V5, V6, I or aVL V1, V2 or V3 V5 or V6

Figure 10.17: ST Segment and T Waves in Left Bundle Branch

Block. (A) The ST segment and T wave are normally opposite in direction
(discordant) from that of the QRS complex when there is uncomplicated left
bundle branch block. Note that the small arrow (pointing to the QRS com-
plex) is opposite in direction to the large arrow, which is pointing to the T
wave. (B) When there is myocardial disease, such as myocardial ischemia or
cardiomyopathy, the ST segments and T waves become concordant and fol-
low the direction of the QRS complex. Note that the small and large arrows
are pointing in the same direction.
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Intraventricular Conduction Defect: Bundle Branch Block 131

A.

B.

Figure 10.18: Rate-Related Left Bundle Branch Block (LBBB). Electrocardiogram (ECG) A shows sinus
rhythm, 83 beats per minute with narrow QRS complexes. ECG B is from the same patient showing sinus tachycardia of
102 beats per minute and LBBB.The LBBB is rate related developing only during tachycardia. Note that after the com-
pensatory pause of the PVC in ECG B, there is narrowing of the QRS complex (arrows) similar to the QRS complex in
ECG A. The long pause after the PVC allows the left bundle branch to recover and conducts the next impulse normally.

V6: In V5 or V6, the ST segment is isoelectric or de-
pressed and the T wave inverted because the termi-
nal portion of the QRS complex is upright.
Primary ST and T wave changes: When the ST seg-
ment and T wave changes are concordant in the setting
of LBBB, they are primary and due to the presence of
an intrinsic myocardial disorder such cardiomyopathy
or myocardial ischemia rather than secondary to the
abnormal activation of the ventricles (Fig. 10.17B).
LBBB may be rate related (Figs. 10.18, 10.19, and
10.20). In rate-related LBBB, the bundle branch block
becomes manifest only when there is tachycardia or
bradycardia. This contrasts with fixed bundle branch
block, which is present regardless of the heart rate.
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132 Chapter 10

Table 10.1 is a diagrammatic representation of the dif- Left-sided precordial lead V6

ferent intraventricular conduction abnormalities using n ST segment depressed
only the minimum leads necessary for diagnosis. n T wave inverted

ECG Findings in LBBB Mechanism

1. Wide QRS complexes measuring 0.12 seconds
Wide QRS complex: When there is LBBB, conduction of
Right-sided precordial lead V1
the electrical impulse to the right bundle branch occurs nor-
n Deep QS or rS complex often with slurring of the mally and conduction of the impulse through the left bundle
downstroke or upstroke of the S wave branch is delayed or interrupted. This results in wide QRS
n Onset of intrinsicoid deflection is normal measuring complexes measuring 0.12 seconds because of asynchro-
0.03 seconds nous activation of the ventricles.
Left sided precordial lead V6 Delayed onset of the intrinsicoid deflection or R peak
n Monophasic R or slurred upstroke of the R wave with time in V5 or V6: The intrinsicoid deflection refers to the
rR, RR, or M-shaped configuration abrupt downward deflection of the R wave on arrival of the
n R peak time or onset of intrinsicoid deflection is pro- impulse at the recording electrode. When there is LBBB, acti-
longed measuring 0.05 seconds vation of the right ventricle is preserved because conduction
through the right bundle branch is intact. Thus the onset of
2. ST segments and T waves are opposite in direction (normally
the intrinsicoid deflection in V1 is normal, measuring 0.03
discordant) to the QRS complexes
seconds. Activation of the left ventricle is delayed because
Right-sided precordial lead V1
there is a block in the left bundle branch. Thus the onset of
n ST segment elevated the intrinsicoid deflection in V5 and V6 is delayed, measuring
n T wave upright 0.05 seconds.

TABLE 10.1

Summary of the ECG Findings of the Different Intraventricular

Conduction Abnormalities
I II III aVL aVF V1 V6

LAFB

LPFB

RBBB

RBBB + LAFB

RBBB + LPFB

LBBB

The table summarizes the different ECG features of the different intraventricular conduction abnor-
malities using only the minimum leads for diagnosis. ECG, electrocardiogram; LAFB, left anterior fasci-
cular block; LPFB, left posterior fascicular block; LBBB, left bundle branch block; RBBB, right bundle
branch block.
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Intraventricular Conduction Defect: Bundle Branch Block 133

A. Baseline ECG

B. LBBB

Figure 10.19: Rate-Related Left Bundle Branch Block (LBBB). (A) A 12-lead electrocardiogram (ECG) ob-
tained a few hours before (B).The QRS complexes are narrow with left axis deviation because of left anterior fascicu-
lar block. (B) ECG from the same patient a few hours later showing LBBB. QS complexes with tall voltages are
present in V1 to V3, which can be mistaken for anteroseptal myocardial infarction or left ventricular hypertrophy.
Marked ST depression is noted in I and aVL and marked ST elevation is noted in V1 to V3, which can be mistaken for
acute coronary syndrome.

Figure 10.20: Bradycardia-Dependent Bundle Branch Block. Rhythm strip showing widening of the QRS
complex (arrow) after a pause from bradycardia-dependent bundle branch block.
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134 Chapter 10
Absence of septal q wave in V5 or V6: Normally, the ventric-
ular septum is activated by the left bundle branch in a left to
right direction (vector 1) resulting in a small septal q wave in V5
or V6 and a small r wave in V1. When there is LBBB, the ventric-
ular septum is no longer activated in a left-to-right direction.
Rather, it is activated by the right bundle branch in a right-to-
left direction, which is the reverse of normal. The normal septal
q wave in V5 or V6 is no longer recorded and should not be pres-
ent when there is LBBB. V1 and V2 may record a small r wave,
representing activation of the right ventricular wall and apex.
The small r wave in V1 does not represent septal activation.
Slurring of the upstroke of the R wave with rR or RR
(M-shaped) configuration of the QRS complex in V6: Af-
ter the right ventricle is activated, the impulse moves from
right ventricle to left ventricle across the interventricular
septum by myocardial cell to myocardial cell conduction.
This results in tall R waves in V6 and deep S waves in V1 and
V2. The initial R wave in V6 represents activation of the ven-
tricular septum, and the larger terminal R deflection repre-
sents activation of the left ventricular free wall. The dip or
notch between the initial R and terminal R is due to activa-
tion of a smaller mass of myocardium between the septum
and left ventricular free wall. Deep S waves often with slurred
downstroke are recorded in V1 and V2.
Absence of terminal r in V1 and absence of terminal s
waves in V6: Whenever there is an intraventricular conduc-
tion abnormality, the area supplied by the blocked bundle
branch is delayed and will be the last to be activated. Because
the left bundle branch supplies the left ventricle and the left
ventricle is located to the left and posterior to the right ven-
tricle, the terminal impulse will be directed to the left and
posteriorly. Right-sided precordial leads such as V1 or V2
should not record a terminal r wave, and left sided precor-
dial leads V5 or V6 should not record a terminal S or s wave.
Rate-related bundle branch block: Bundle branch block,
left or right, may be rate related before it becomes fixed.
When LBBB is rate related, LBBB occurs only when the heart
rate becomes increased or decreased. When LBBB is fixed or
permanent, LBBB persists regardless of the heart rate.
Bradycardia-dependent bundle branch block: In
bradycardia-dependent bundle branch block, RBBB or
LBBB occurs only when there is bradycardia or slowing of
the heart rate. Bradycardia-dependent bundle branch
block is due to phase 4 diastolic depolarization, which is
inherently present in cells with automatic properties,
including cells within the intraventricular conduction
system. When there is a long R-R interval, cells with auto-
matic properties undergo spontaneous phase 4 diastolic
depolarization resulting in a transmembrane potential
that slowly becomes less and less negative. Thus, the sinus
impulse may not be able to conduct across a bundle
branch that is partially depolarized.
Tachycardia-related bundle branch block: The re-
fractory period of one bundle branch is usually longer
than the refractory period of the other bundle branch.
When the heart rate is relatively slow, both bundle
branches are given enough time to repolarize. However,
when the heart rate is faster, the impulses may arrive well
before the bundle branch with a longer refractory period
has a chance to recover. This may result in bundle branch
block that is evident during tachycardia, that resolves
when the heart rate slows down to baseline. The longer
refractory period of one bundle branch is due to its longer
action potential duration when compared with the other
bundle branch. This type of rate-related bundle branch
block is called phase 3 aberration.
Clinical Significance
Unlike the right bundle branch, which is long and thin, the
left bundle branch immediately divides into two main fasci-
cles: the left anterior and left posterior fascicles. A midseptal
branch also exists, although there are no criteria diagnostic
of a midseptal lesion. LBBB therefore is an example of bifas-
cicular block. LBBB can occur in the main left bundle (predi-
visional) or at the level of the fascicles (postdivisional). It can
also occur at the level of the bundle of His.
Clinical significance: LBBB can occur as an isolated finding
in normal, asymptomatic individuals without evidence of
cardiac disease but is rare.
In a study of 122,043 asymptomatic and healthy airmen,
only 17 individuals were noted to have LBBB compared
with 231 with RBBB. In this study, none of 44,231 men
younger than age 25 had LBBB.
In another study of 110,000 individuals, isolated LBBB
occurred in 112 cases (0.1%) without apparent or sus-
pected heart disease, compared with 198 cases of isolated
RBBB (0.28%). The overall mortality in patients with iso-
lated LBBB was not increased when compared with pa-
tients with RBBB during a mean follow-up of 9.5 years.
However, patients with isolated LBBB but not RBBB had
increased risk of developing overt cardiovascular disease,
which may, in the long run, translate into a higher mor-
bidity and mortality.
n In the Framingham study, 55 of 5,209 individuals
(1%) developed new-onset LBBB during a follow-up
period of 18 years. The mean age of onset was 62
years. LBBB was associated with hypertension (de-
fined as blood pressure of 160/95 mm Hg), ischemic
heart disease, or primary myocardial disease among
47 of the 55 patients. Only 9 of 55 patients (16%) were
free of cardiovascular disease during a mean follow-
up period of 6 years after the onset of LBBB.
n A 40-year follow-up study of 17,361 subjects in
Hiroshima and Nagasaki, Japan, who underwent bien-
nial health examinations showed 110 subjects with
LBBB. The average age at diagnosis was 69.6 10
years in men and 68.3 10.9 years in women, with
progressive increase in the incidence of LBBB with
age. There was a higher incidence of hypertension,
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Intraventricular Conduction Defect: Bundle Branch Block
ischemic heart disease, left ventricular hypertrophy
with ST-T abnormalities, and increased cardiotho-
racic ratio among patients who developed LBBB when
compared with controls. Age at death was similar for
patients with LBBB and controls, although mortality
from congestive heart failure and myocardial infarc-
tion was significantly higher in patients with LBBB.
n Finally, among 723 asymptomatic patients with normal
left ventricular ejection fraction incidentally diagnosed
to have bundle branch block (58.1% LBBB and 41.9%
RBBB) in a community-based patient population, retro-
spective analysis of computerized medical records after
24 years follow-up showed that isolated bundle branch
block is not a benign finding. Cardiac-related morbidity
and mortality is similar to patients with known conven-
tional risk factors without bundle branch block.
Etiology:LBBB is an acquired conduction disorder and is usu-
ally a marker of an underlying cardiac abnormality in contrast
to RBBB, which may be congenital and may remain as an iso-
lated finding. The majority of patients with LBBB, but not
RBBB, have cardiac disease. If cardiac disease is not apparent, it
is very likely that overt cardiac abnormality will subsequently
develop. The common causes of LBBB include hypertension,
coronary artery disease, valvular diseases (especially aortic
stenosis), cardiomyopathy, acute myocarditis, and degenerative
disease of the conduction system. LBBB is generally a marker
of left ventricular disease and is the most common conduction
abnormality in patients with primary cardiomyopathy.
Hemodynamic abnormalities: LBBB can diminish cardiac
performance even in the absence of associated myocardial
disease. In LBBB, the ventricles are activated sequentially
rather than synchronously. Thus, left and right ventricular
contraction is not simultaneous. Furthermore, because con-
duction of the impulse within the left ventricle is by direct
myocardial spread, contraction of the left ventricle is not
synchronized and can result in wall motion abnormalities.
Mitral regurgitation can occur when the two papillary mus-
cles are not simultaneously activated. The significance of
these contraction abnormalities may not be apparent in pa-
tients with reasonably good left ventricular systolic function.
However, in patients who have myocardial disease and severe
left ventricular dysfunction, the presence of LBBB can make
systolic dysfunction even more pronounced.
LBBB makes diagnosis of certain disorders difficult:
When LBBB is present, the ECG becomes unreliable as a di-
agnostic tool for identifying a variety of clinical entities.
Left ventricular hypertrophy: Left ventricular hyper-
trophy will be difficult to diagnose when there is LBBB be-
cause of the tall voltage and secondary ST-T changes asso-
ciated with LBBB. Nevertheless, approximately 85% of
patients with LBBB will have left ventricular hypertrophy.
Acute MI: Acute MI is difficult to diagnose when LBBB is
present because q waves and ST-T abnormalities associ-
ated with acute MI can be obscured by the LBBB. Con-
versely, when LBBB is present, Q waves or QS complexes
135
may occur in the anterior precordial leads and may mimic
a myocardial infarct. The ST-T changes of LBBB can also
be mistaken for current of injury (see acute MI and LBBB
Chapter 23, Acute Coronary Syndrome: ST Elevation
Myocardial Infarction). The following findings suggest
the presence of MI when there is LBBB.
n Acute MI should be suspected when there is concor-
dant ST segment depression or concordant ST seg-
ment elevation 1 mm in a patient with symptoms of
myocardial ischemia. Concordant ST segment depres-
sion is present when the QRS complex is negative and
the ST segment is depressed. Concordant ST segment
elevation is present when the QRS complex is positive
and the ST segment is elevated.
n Acute MI should also be suspected when there is dis-
cordant ST segment elevation 5 mm accompanied
by symptoms of ischemia. This implies that ST seg-
ment elevation of at least 5 mm is present in leads
with deep S waves such as V1, V2, or V3.
n Notching of the upstroke of the S wave in V3 or V4,
also called Cabrera sign, or the upstroke of the R wave
in V5 or V6, also called Chapman sign, are highly spe-
cific but not very sensitive for MI.
n Q waves in leads V5 or V6 or leads located at the left
side of the ventricular septum (I or aVL) indicate an
MI, which may be recent or remote.
During stress testing: LBBB can cause a false-positive
or a false-negative stress test.
n ECG stress testing: During stress testing, LBBB may
mask the ECG changes of myocardial ischemia result-
ing in a false-negative stress test. Conversely, LBBB can
result in a false-positive stress test because it can cause
secondary ST-T changes in the ECG, which may be mis-
interpreted as being due to ischemia. Thus, the American
College of Cardiology/American Heart Association
guideline on chronic stable angina does not recommend
stress testing in patients with LBBB using ECG alone as
a marker for myocardial ischemia. This is a Class III in-
dication, meaning that there is evidence that the proce-
dure is not useful. Stress testing of patients with com-
plete LBBB on baseline ECG should always include an
imaging modality, preferably a nuclear perfusion scan.
n Stress testing with imaging: Nuclear scan uses perfu-
sion mismatch, whereas echo uses wall motion ab-
normality as the end point for detecting myocardial
ischemia. Because left ventricular wall motion abnor-
malities inherently occur when there is LBBB, a nu-
clear perfusion scan is preferred over echocardiogra-
phy as the imaging modality during stress testing.
Pharmacologic stress testing is preferred over exercise
when LBBB is present because exercise can further
augment the wall motion abnormalities of LBBB even
in the absence of ischemia. Dipyridamole or adeno-
sine (but not dobutamine) are preferred because both
agents do not alter contractility.
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136 Chapter 10
n Auscultatory findings: The presence of LBBB will
delay closure of the mitral and aortic valves. This will
cause the first heart sound to become single and the
second heart sound to be paradoxically split. When
paradoxical splitting of the second heart sound is pres-
ent, the second heart sound becomes single or nar-
rowly split with inspiration and widely split with expi-
ration. This pattern is the opposite of normal. A short
murmur of mitral regurgitation may be audible during
early systole because of asynchrony in contraction of
the papillary muscles. The presence of mild mitral re-
gurgitation from LBBB, however, is better shown with
color Doppler imaging during echocardiography.
Treatment
LBBB is usually associated with cardiac disease more com-
monly coronary disease, hypertension, valvular disease, or
cardiomyopathy. Overall treatment depends on the underly-
ing cardiac condition. In completely asymptomatic patients
without known cardiac disease, no treatment is required.
LBBB is a bifascicular block that may progress to trifascicular
block or complete AV block. In patients with trifascicular
block, insertion of a permanent pacemaker is warranted
(see Chapter 11, Intraventricular Conduction Defect: Trifas-
cicular Block; see also the American College of Cardiology/
American Heart Association/Heart Rhythm Society guide-
lines on permanent pacemaker implantation in patients with
bifascicular and trifascicular block).
Patients with systolic left ventricular dysfunction who con-
tinue to have symptoms of heart failure despite receiving opti-
mal medical therapy may benefit from cardiac resynchroniza-
tion therapy if they have LBBB. Cardiac resynchronization
involves insertion of a biventricular pacemaker that can stim-
ulate both right and left ventricles simultaneously. Pacing both
ventricles simultaneously significantly decreases the delay in
the spread of electrical impulse in patients with wide QRS
complexes and has been shown to improve cardiac output and
diminish mitral regurgitation. The patient should be in nor-
mal sinus rhythm so that timing of atrial and ventricular con-
traction can be synchronized. Although most patients who
have received biventricular pacemakers have LBBB, the width
of the QRS complex rather than the type of bundle branch
block is the main indication for biventricular pacing. Patients
who are candidates for cardiac resynchronization therapy
should have all of the following features:
Patients with wide QRS complexes (0.12 seconds)
Normal sinus rhythm
Systolic dysfunction (ejection fraction 35%) because of
ischemic or nonischemic cardiomyopathy
New York Heart Association functional class III or IV
heart failure
Patients continue to have heart failure in spite of optimal
medical therapy
Prognosis
Similar to RBBB, the overall prognosis depends on the etiol-
ogy of the LBBB.
In the Framingham study, patients who did well were
those with normal axis of the QRS complex (to the right
of 0), those without any left atrial abnormality or left
atrial conduction delay and those who did not have
changes in the ECG before the development of LBBB.
Among older patients with LBBB, majority had an-
tecedent cardiomegaly, hypertension, or coronary disease.
If they did not have any of these findings, the majority
went on to develop one of these cardiovascular abnormal-
ities. The presence of these cardiovascular diseases will
translate into a higher mortality.
Finally, long-term follow-up studies show that patients
with LBBB have a higher incidence of cardiovascular dis-
ease with higher mortality from congestive heart failure
and acute MI, although all-cause mortality may not be
significantly different among patients with LBBB com-
pared with those who do not.
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Trevino AJ, Beller BM. Conduction disturbance of the left bun-
dle branch system and their relationship to complete heart
block II.A review of differential diagnosis, pathology and
clinical significance. Am J Med. 1971;51:374382.
Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for
intraventricular conduction disturbances and pre-excitation.
J Am Coll Cardiol. 1985;5:12611275.
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11
Intraventricular Conduction
Defect: Trifascicular Block
Trifascicular Block
Types of intraventricular conduction defect: In-
stead of two main branches, the bundle of His can be
simplified as dividing into three discrete pathways;
namely, the right bundle branch, the left anterior, and
the left posterior fascicles. Thus, the following abnor-
malities can occur:
Unifascicular block (block involves one fascicle):
n Left anterior fascicular block (LAFB)
n Left posterior fascicular block (LPFB)
n Right bundle branch block (RBBB)
Bifascicular block (block involves two fascicles):
n Left bundle branch block (LBBB)
n RBBB  LAFB
n RBBB  LPFB
Definite trifascicular block (block involves all
three fascicles). The following are examples of defi-
nite trifascicular block.
n Alternating bundle branch block
n RBBB  alternating fascicular block
n RBBB  Mobitz type II second-degree atrioven-
tricular (AV) block
n LBBB  Mobitz type II second-degree AV block
Possible trifascicular block: The following are ex-
amples of possible trifascicular block.
n Complete AV block with ventricular escape
rhythm
n Any bifascicular block  first-degree or second-
degree AV block
n RBBB  LAFB  first-degree or second-de-
gree AV block
n RBBB  LPFB  first-degree or second-de-
gree AV block
n LBBB  first-degree or second-degree AV block
Nonspecific intraventricular block: This type of
electrocardiogram (ECG) abnormality does not
conform to any of the above intraventricular blocks.
138
Trifascicular block indicates that some form of con-
duction abnormality is present in all three fascicles.
The conduction abnormality may be due to simple de-
lay (first-degree block), intermittent block (second-
degree block), or complete interruption (third-degree
block) of the sinus impulse to all three fascicles. Trifas-
cicular block does not imply that the block is always
complete in all three fascicles.
Bilateral Bundle Branch Block
Alternating bundle branch block: Whether it is a
RBBB alternating with LBBB, or a RBBB recorded at
one time and a LBBB recorded at some other time,
such a block would constitute a trifascicular block be-
cause there is evidence that both bundle branches, and
therefore all three fascicles of the conduction system,
are involved. Example of RBBB and LBBB occurring in
the same patient is shown in Figure 11.1. Another
example of LBBB and RBBB occurring in the same
patient is shown in Figure 11.2A, B. When LBBB and
RBBB occur in the same patient, bilateral bundle
branch block is present. This is an example of trifas-
cicular block.
RBBB  alternating fascicular block: When RBBB is
fixed and is accompanied by LAFB that alternates with
LPFB, a trifascicular block is present because all three
fascicles are involved (Fig. 11.3). This is a rare presenta-
tion of trifascicular block.
RBBB or LBBB  Mobitz type II second-degree AV
block: Mobitz type II second-degree AV block is an in-
franodal block (see Chapter 8, Atrioventricular Block).
When there is RBBB or LBBB with a type II second-de-
gree AV block, the AV block is at the level of the His-
Purkinje system. Thus, a RBBB or LBBB with a type II
second-degree AV block suggests the presence of a tri-
fascicular block (Fig. 11.4).
Complete AV block with ventricular escape
rhythm: The ultimate manifestation of trifascicular
block is complete block involving all three fascicles or
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Intraventricular Conduction Defect: Trifascicular Block 139

A.

B.

Figure 11.1: Bilateral Bundle Branch Block. Electrocardiogram (ECG) A and ECG B are from the same
patient taken 6 months apart. (A) Right bundle branch block (RBBB) with left anterior fascicular block. (B) Left bun-
dle branch block (LBBB) with type II second-degree AV block. The presence of RBBB and LBBB in the same patient
suggests bilateral bundle branch block. (B) also shows Mobitz type II second-degree AV block. Mobitz type II
second-degree AV block in addition to LBBB is also indicative of trifascicular block.

both bundle branches. When this occurs, only a ven-
tricular escape impulse can maintain the cardiac
rhythm (Fig. 11.5A). Complete AV block with ventric-
ular escape rhythm is most often a trifascicular block.
However, should the complete block occur at the level
of the AV node, it would not constitute a trifascicular
block.
Complete AV block with ventricular escape
rhythm: Another example of complete AV block with
ventricular escape rhythm is shown in Figure 11.6. The
initial ECG showed LBBB with first-degree AV block.
When a bifascicular or trifascicular block deteriorates
into complete AV block with ventricular escape
rhythm, the AV block is almost always trifascicular.
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140 Chapter 11

A.

B.

Figure 11.2: Bilateral Bundle Branch Block. (A, B) From the same patient. The initial electrocardiogram
(ECG) (A) shows left bundle branch block (LBBB) with deep S waves in V1. Subsequent ECG taken a year later (B)
shows right bundle branch block (RBBB)  left anterior fascicular block. The presence of LBBB and RBBB in the same
patient is consistent with bilateral bundle branch block. Note also that there is first-degree atrioventricular block in
both ECGs, which in the presence of bifascicular block, is also indicative of trifascicular block.
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Intraventricular Conduction Defect: Trifascicular Block 141

Figure 11.3: Fixed Right Bundle Branch Block (RBBB)  Left Anterior Fascicular Block Alternat-
ing with Left Posterior Fascicular Block. The precordial leads show RBBB. The frontal leads show left ante-
rior fascicular block alternating with left posterior fascicular block. This conduction abnormality is an example of
trifascicular block.

Any bifascicular block  first-degree or second-
degree AV block: RBBB  LAFB  second-degree AV
block (Fig. 11.7), RBBB  LPFB  second-degree AV
block (Fig. 11.8), and LBBB  second-degree AV block
are all possible examples of trifascicular block. Bifascic-
ular block with second-degree AV block is not always
the result of trifascicular block because the AV block can
occur at the AV node instead of the remaining fascicle.
When there is a bifascicular block such as RBBB 
LAFB, the only pathway by which the atrial impulse can
reach the ventricles is through the remaining posterior
fascicle. Note that the atrial impulse may be delayed or
interrupted at the level of the AV node or at the distal
conducting system resulting in first-degree or second-
degree AV block. Should the first-degree or second-de-
gree AV block involve the remaining fascicle, a trifascic-
ular block would be present. Should the first-degree or
second-degree AV block occur at the AV node, it would
not qualify as a trifascicular block. This latter condition
must therefore be excluded before diagnosing a trifasci-
cular block. RBBB  LAFB  type I second-degree AV
block is shown in Figure 11.9. This is usually an AV
nodal block, but it is also possible that the block is tri-
fascicular, involving the remaining fascicle.

Figure 11.4: Mobitz Type II Second-Degree Atrioventricular (AV) Block. Mobitz type II second-degree
AV block is a disease of the distal conduction system.The rhythm strip above was recorded in lead V1. It shows right
bundle branch block (RBBB) and second-degree AV block with a fixed PR interval from Mobitz type II AV block. The
presence of RBBB and Mobitz type II AV block is consistent with trifascicular block.
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142 Chapter 11

A.

B.

Figure 11.5: Complete Atrioventricular (AV) Block with Ventricular Escape Rhythm. Electrocardiogram
(ECG) A shows complete AV block with ventricular escape rhythm. ECG B was obtained from the same patient sev-
eral hours earlier showing right bundle branch block  left anterior fascicular block. The presence of ventricular
escape rhythm and a previous ECG showing bifascicular block suggests that the complete AV block is infranodal.
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Intraventricular Conduction Defect: Trifascicular Block 143

A.

B.

Figure 11.6: Complete Atrioventricular (AV) Block with Ventricular Escape Rhythm.
Electrocardiogram (ECG) (A) shows complete AV block with ventricular escape rhythm. The P waves are
nonconducted (arrows). ECG (B) taken 2 months earlier shows left bundle branch block with first-degree AV block,
which is consistent with trifascicular block.
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144 Chapter 11

Figure 11.7:Right Bundle Branch Block (RBBB)  Left Anterior Fascicular Block (LAFB)  Second-
Degree Atrioventricular (AV) Block. This 2:1 second-degree AV block combined with RBBB and LAFB is
almost always a trifascicular block.

Figure 11.8:Right Bundle Branch Block (RBBB)  Left Posterior Fascicular Block (LPFB)  Second-
Degree Atrioventricular (AV) Block. A 2:1 second-degree AV block in association with RBBB and LPFB is
almost always a trifascicular block.
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Figure 11.9: Right Bundle Branch Block (RBBB)  Left Anterior Fascicular Block (LAFB) 
First-Degree and Second-Degree Atrioventricular (AV) Block  Trifascicular Block. The 12-lead
electrocardiogram (ECG) shows RBBB  LAFB. There is also first-degree and type I second-degree AV block (arrow).
This combination of ECG abnormalities may be due to trifascicular block.
Complete AV block resulting from trifascicular block
is invariably fatal unless a permanent pacemaker is
implanted. The presence of trifascicular disease there-
fore should be recognized so that a permanent pace-
maker can be implanted before the conduction ab-
normality progresses to complete AV block.
Bifascicular or trifascicular block with subsequent de-
velopment of intermittent or persistent complete AV
block is a Class I indication for permanent pacemaker
implantation regardless of the presence or absence
of symptoms according to American College of
Cardiology/American Heart Association/Heart Rhythm
Society guidelines.
ECG Findings in Trifascicular Block
1. The following are definite examples of trifascicular block:
Alternating bundle branch block
RBBB  alternating fascicular block
RBBB  Mobitz type II second-degree AV block
LBBB  Mobitz type II second-degree AV block
2. The following are possible examples of trifascicular block:
Bifascicular block  first-degree AV block
RBBB  LAFB  first-degree AV block
RBBB  LPFB  first-degree AV block
LBBB  first-degree AV block
Intraventricular Conduction Defect: Trifascicular Block 145
Bifascicular block  second-degree AV block
RBBB  LAFB  second-degree AV block
RBBB  LPFB  second-degree AV block
LBBB  second-degree AV block
Complete AV block with ventricular escape rhythm
Mechanism
Definite trifascicular block:
Alternating bundle branch block: Before complete AV
block develops, trifascicular block may manifest as a more
subtle abnormality, such as RBBB alternating with LBBB.
When this occurs, a delay in the impulse (first-degree
block) in one bundle branch alternates with delay in the
other bundle branch, resulting in alternating bundle
branch block. The presence of RBBB alternating with LBBB
suggests disease of both bundle branches and is consistent
with bilateral bundle branch block or trifascicular block.
RBBB  alternating fascicular block: RBBB is con-
stantly present in the precordial leads with the axis in the
frontal plane alternating between left axis deviation
30 and right axis deviation 90. This is due to a de-
lay in one fascicle alternating with a delay in the other fas-
cicle. This is consistent with trifascicular block.
Type II second-degree AV block: If LBBB or RBBB
(with or without fascicular block) is associated with type II
second-degree AV block, it is very likely that there is bilateral
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146 Chapter 11
bundle branch block because type II second-degree AV
block involves only the distal conduction system.
Possible trifascicular block:
Bifascicular block  first-degree or second-degree
AV block: First-degree AV block as well as type 1 second-
degree AV block can occur anywhere within the conduc-
tion system including the AV node or more distally within
the bundle branches or fascicles. When AV block occurs in
the setting of bifascicular block, the AV block may involve
the third or remaining fascicle, in which case a trifascicu-
lar block would be present. It is also possible that the AV
block may not be in the third fascicle, but at the level of
the AV node, in which case it would not be a trifascicu-
lar block. The block is trifascicular only if the first-
degree or second-degree AV block involves the remaining
fascicle.
Complete AV block with ventricular escape rhythm:
Trifascicular block is present when there is simultaneous
block involving both bundle branches or all three fascicles
of the conduction system. The ECG will show complete
AV block. The escape rhythm can originate only from the
ventricles. If bifascicular or trifascicular block is present
in previous ECGs, complete AV block with a ventricular
escape rhythm is almost always the result of a block in the
His-Purkinje system.
Clinical Implications
Patients with trifascicular block are at risk for developing
complete AV block. The AV block can occur suddenly and
can result in syncope (Stokes-Adams syndrome) or sudden
death. The presence of trifascicular block should be recog-
nized before complete AV block develops.
When complete AV block occurs, the level of the AV block
should always be localized. AV block at the level of the AV node
is often reversible and has a better prognosis than AV block oc-
curring more distally at the level of the His-Purkinje system.
The patients history, previous ECG, presence and location of
the acute myocardial infarction (MI), and the origin of the
escape rhythm are helpful in localizing the level of the AV
block.
History: The block is most likely AV nodal if the patient
gives a history of taking medications that can block the
AV node such as beta blockers, calcium channel blockers
(verapamil and diltiazem), and digitalis.
Previous ECG: The presence of distal conduction system
disease such as bundle branch block, bifascicular block, or
trifascicular block suggest that the AV block is in the dis-
tal conduction system.
Acute MI: When acute MI is associated with AV block,
the AV block is at the level of the AV node if the MI is in-
ferior. It is infranodal and at the level of the His-Purkinje
system if the MI is anterior.
Escape rhythm: When the AV block is infranodal, the es-
cape rhythm is always ventricular. When the AV block is at
the level of the AV node, the escape rhythm is usually AV
junctional.
The presence of bundle branch block (especially LBBB) may
be a marker of severe myocardial disease and left ventricular
systolic dysfunction. When a patient with bifascicular or tri-
fascicular block presents with syncope, progression to com-
plete AV block is likely. However, one should not overlook the
possibility that ventricular tachycardia rather than complete
AV block may be the cause of the syncope. Insertion of a per-
manent pacemaker to prevent bradyarrhythmia may not alter
the prognosis of patients with severe myocardial disease if the
cause of the syncope is a ventricular arrhythmia.
The causes of trifascicular block include idiopathic car-
diomyopathy, ischemic heart disease, hypertension, valvular
heart diseases (especially calcific aortic stenosis), fibrosis or
calcification of the conduction system, infiltrative cardiac
diseases such as sarcoidosis, hypothyroidism, myocarditis,
and other inflammatory heart diseases such as Dengue fever,
diphtheria, leishmania, and Lyme disease.
Treatment
The following are the indications for implantation of permanent
pacemakers in patients with chronic bifascicular and trifascicular
block according to the American College of Cardiology/American
Heart Association/Heart Rhythm Society guidelines.
Class I: Condition in which there is evidence or agreement that
a given procedure or treatment is useful and effective.
Symptomatic and Asymptomatic Patients:
1. Advanced second-degree or intermittent third-degree AV block
2. Type II second-degree AV block
3. Alternating bundle branch block
Class IIa: The weight of evidence is in favor of usefulness or ef-
ficacy of a procedure or treatment.
Symptomatic Patients:
1. Syncope not demonstrated to be due to AV block when other
likely causes have been excluded, specifically ventricular
tachycardia.
Asymptomatic Patients:
1. Incidental finding at electrophysiological study of markedly
prolonged HV interval (100 milliseconds).
2. Incidental finding at electrophysiological study of pacing in-
duced infra-His block that is not physiological.
Class IIb: Usefulness or efficacy of the procedure or treat-
ment is less well established.
Symptomatic or Asymptomatic Patients:
1. Neuromuscular diseases with bifascicular block or any fascic-
ular block with or without symptoms. These include my-
otonic muscular dystrophy, Erb dystrophy, and peroneal mus-
cular atrophy.
Class III: The procedure is not useful or effective and in some
cases may be harmful.
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Asymptomatic Patients:
Permanent pacemaker implantation is not indicated for:
1. Fascicular block without AV block or symptoms.
2. Fascicular block with first-degree AV block without symptoms.
Complete AV block involving the distal conducting system is
often sudden and unexpected. Thus, the ECG manifestations
of trifascicular block should be recognized before complete
AV block becomes manifest. When there is evidence of trifas-
cicular block, a permanent pacemaker should be inserted,
even in asymptomatic patients, because there is no effective
medical therapy for complete AV block at the level of the dis-
tal conduction system.
Therapy should target the underlying cause of the conduc-
tion abnormality, such as ischemic cardiomyopathy, hy-
pothyroidism, sarcoidosis, myocarditis, or other inflamma-
tory diseases. Whenever there is a need for permanent pacing
in patients with bifascicular or trifascicular disease, left ven-
tricular systolic function should be evaluated with an imag-
ing procedure such as echocardiography. In this era of ad-
vanced technology, the need for permanent pacing for
bradycardia should also take into consideration the need for
biventricular pacing and automatic defibrillation in patients
with severe left ventricular systolic dysfunction.
Prognosis
Prognosis depends on the cause of the trifascicular block. If
the conduction abnormality is an isolated abnormality
resulting from sclerosis or degenerative disease of the con-
Intraventricular Conduction Defect: Trifascicular Block 147
duction system, prognosis after insertion of a permanent
pacemaker is the same as for patients without the conduc-
tion abnormality. Most patients with trifascicular disease
may have associated myocardial disease. The prognosis of
these patients depends on the etiology of the conduction
abnormality.
Suggested Readings
Dunn MI, Lipman BS. Abnormalities of ventricular conduction:
fascicular block, infarction block, and parietal block. In:
Lippman-Massie Clinical Electrocardiography. 8th ed. Chicago:
Yearbook Medical Publishers, Inc; 1989:148159.
Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a Report of the American College of Cardiology/
American Heart Association Task Force on Practice Guide-
lines (Writing Committee to Revise the ACC/AHA/NASPE
2002 Guideline Update for Implantation of Cardiac Pace-
makers and Antiarrhythmia Devices). J Am Coll Cardiol.
2008;51:2085-2105.
Marriott HJL. The hemiblocks and trifascicular block. In:
Practical Electrocardiography. 5th ed. Baltimore: The Williams
and Wilkins Company; 1972:8694.
Sgarbossa EB, Wagner GS. Electrocardiography: In: Topol EJ, ed.
Textbook of Cardiovascular Medicine. 2nd ed. Philadelphia:
Lippincott Williams & Wilkins; 2002:13301354.
Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for
intraventricular conduction disturbances and pre-excitation.
J Am Coll Cardiol. 1985:12611275.
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12
Sinus Node Dysfunction
Sick Sinus Syndrome
The sinus node is the pacemaker of the heart. It con-
tains cells with automatic properties that are capable of
generating electrical impulses. When the sinus node
discharges, it does not leave any imprint in the electro-
cardiogram (ECG). The sinus impulse is recognized
only when it has propagated to the atria causing a small
deflection called a P wave. The impulse from the sinus
node is called normal sinus rhythm.
Sinus node dysfunction: Sinus node dysfunction oc-
curs when the sinus node fails to function as the pace-
maker of the heart. Slowing of the heart because of sinus
node dysfunction should not be confused with slowing
of the heart because of atrioventricular (AV) block.
Sinus dysfunction: When the sinus node com-
pletely fails as the pacemaker of the heart, a long pe-
riod of asystole will occur. The ECG will record a
long flat line without P waves (Fig. 12.1A). The long
pause is frequently terminated by escape complexes
from the atria or ventricles.
AV block: When there is complete AV block, sinus P
waves are present, but are not conducted to the ven-
tricles. The presence of sinus P waves indicates that
A Sinus Node Dysfunction
B AV Block
Figure 12.1: Sinus Node Dysfunction versus Atrioven-
tricular (AV) Block. (A) When bradycardia or asystole is due
to sinus node dysfunction, no P waves will be recorded in the
electrocardiogram. (B) When bradycardia or ventricular asystole
is due to AV block, sinus P waves are present but are not
followed by QRS complexes because the atrial impulses are
blocked on their way to the ventricles.
148
the sinus node is functioning normally and is gener-
ating impulses that conduct to the atria, but is
blocked on its way to the ventricles (Fig. 12.1B).
Sinus node dysfunction: Sinus node dysfunction can
be due to intrinsic or extrinsic causes.
Intrinsic causes of sinus node dysfunction: In-
trinsic disease of the sinus node is associated with
structural changes in the sinus node itself or the sur-
rounding atria resulting in progressive deterioration
in sinus node function. This may be due to ischemia,
inflammation, infection, infiltrative, metastatic or
rheumatic diseases, surgical injury, collagen disease,
sclerosis, fibrosis, or idiopathic degenerative diseases
that often involve the whole conduction system.
Sinus node dysfunction can be manifested by a num-
ber of arrhythmias, although the underlying rhythm
disorder is always a bradycardia. About half of all
permanent pacemakers in the United States are im-
planted because of sinus node dysfunction. Before
sinus node dysfunction is attributed to sick sinus
syndrome, which is progressive and usually irre-
versible, extrinsic causes, which are reversible, should
be excluded.
Extrinsic and reversible sinus node dysfunc-
tion: The sinus node can be suppressed by neuro-
cardiogenic reflexes; enhanced vagal tone; hy-
pothermia; hypoxia and hypercapnia (especially
during sleep apnea); increased intracranial pressure;
hypothyroidism; hyperkalemia; and drugs that can
suppress the sinus node such as lithium, amitripty-
line, clonidine, methyldopa, beta blockers, nondihy-
dropyridine calcium channel blockers, amiodarone,
sotalol, and digitalis. Sinus suppression from extrin-
sic causes is usually reversible and should be differ-
entiated from intrinsic disease of the sinus node.
Arrhythmias associated with sick sinus syn-
drome: Sick sinus syndrome should be suspected
when any of the following arrhythmias occur. Except
for the tachycardia-bradycardia syndrome, these ar-
rhythmias may be difficult to differentiate from extrin-
sic and reversible causes of sinus node dysfunction.
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Figure 12.2: Sinus Bradycardia. The rhythm is sinus bradycardia with a rate of 42 beats per minute. Although
sinus bradycardia is commonly seen in normal healthy and well-conditioned individuals, the slow sinus rate may
also be a sign of sick sinus syndrome.
Inappropriate sinus bradycardia
Sinus arrest, sinus pause, and sinoatrial (SA) exit
block
Tachycardia-bradycardia syndrome
Chronic atrial fibrillation
Escape rhythms arising from the atria, AV junction,
or ventricles
Inappropriate sinus bradycardia: When there is
structural disease of the sinus node, one of the mani-
festations is abnormal slowing of the sinus rate, result-
ing in sinus bradycardia. Sinus bradycardia is defined
as a sinus rate of 60 beats per minute (bpm). It is a
normal finding during rest or sleep. Sinus bradycardia
is seldom a cause of concern until it becomes unusually
slow at 50 bpm. Sinus bradycardia of 40 to 50 bpm is
often seen in normal healthy, well-conditioned athletes
(Fig. 12.2). Thus, marked sinus bradycardia occurring
in healthy individuals may be difficult to differentiate
from inappropriate sinus bradycardia occurring in pa-
tients with sick sinus syndrome. The sinus bradycardia
is inappropriate when it is unusually slow, is persistent,
and does not increase sufficiently with exercise. For ex-
ample, sinus bradycardia of 50 bpm may be appropri-
ate for a patient who is asleep, but not for an individual
who is physically active.
Chronotropic incompetence: A patient with sick si-
nus syndrome may or may not be bradycardic at rest,
although there may be failure of the heart rate to in-
crease sufficiently with exercise or with physical activity
because of chronotropic incompetence. Chronotropic
incompetence is diagnosed during exercise testing
when the patient is unable to reach a heart rate equiva-
lent to at least 80% of the maximum heart rate pre-
dicted for the patients age. Although chronotropic in-
competence may be a manifestation of sick sinus
syndrome, there are so many other causes of failure to
reach a certain target heart rate during exercisemost
commonly, the use of pharmacologic agents that can
suppress the sinus node (beta blockers and calcium
channel blockers) as well as autonomic influences. Pa-
tients with chronotropic incompetence resulting from
sick sinus syndrome with symptoms of low cardiac out-
put is a Class I indication for permanent pacing accord-
Sinus Node Dysfunction 149
ing to the American College of Cardiology (ACC),
American Heart Association (AHA), and Heart Rhythm
Society (HRS) guidelines on implantation of permanent
pacemakers.
Sinoatrial Exit Block
Sinoatrial exit block and sinus arrest: Another
manifestation of sinus node dysfunction is failure of
the sinus impulse to conduct to the atria (SA exit
block) or failure of the sinus node to generate an im-
pulse (sinus arrest).
Sinoatrial exit block: In SA exit block, the sinus
node continues to discharge at regular intervals, but
some impulses are blocked and are unable to reach
the surrounding atria. This can result in complete
absence of an entire P-QRS-T complex. If two or
more consecutive sinus impulses are blocked, the
long P-P intervals representing the pauses are exact
multiples of the shorter P-P intervals representing
the basic rhythm (Fig. 12.3). The long pauses should
be terminated by another sinus impulse and not by
an escape complex, so that the P-P intervals can be
measured. Thus, in SA exit block, a mathematical
relation exists between the shorter P-P intervals and
the long pauses.
Sinus arrest: In sinus arrest, the sinus node is un-
able to generate impulses regularly. Because the
abnormality is one of impulse formation rather
SA Exit Block: Distance A = Distance B
B A
Figure 12.3: Sinoatrial Exit Block. In sinoatrial exit block,
the P-P interval straddling a pause (A) is equal to two basic P-P
intervals (B). The red heart represents an entire P-QRS-T that is
missing.
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150 Chapter 12
Sinus Arrest: Distance A is longer than distance B
B A
Figure 12.4: Sinus Arrest. The long pause (A) contains a
P-P interval that is not equal to two basic P-P intervals (B). The
pause represents sinus arrest.
than impulse conduction, the pauses represented by
the long P-P intervals, are not exact multiples of the
shorter P-P intervals representing the basic sinus
rhythm (Fig. 12.4).
Sinus pause: Sinus pause and sinus arrest are similar
and either one can be used interchangeably to describe
the other. Additionally, sinus arrest may be difficult to
differentiate from SA exit block when the P-P intervals
are irregular, such as when there is sinus arrhythmia or
when an escape complex terminates a pause (Fig. 12.5).
When these occur, the pause is simply a sinus pause
because it cannot be identified as sinus arrest or exit
block (Figs. 12.6 and 12.7).
Sinoatrial exit block: Similar to AV block, SA exit block
can be divided into first-degree, second-degree, and
third-degree block. First- and third-degree SA exit block
are not recognizable in the surface ECG because the si-
nus node does not leave any imprint when it discharges.
Only second-degree SA exit block can be identified.
Second-degree SA exit block: Second-degree SA
exit block is further subdivided into type I, also called
SA Wenckebach, and type II, SA exit block. The differ-
ence between type I and type II exit block is shown in
Figure 12.8B, C.
Sinoatrial Wenckebach
SA Wenckebach: Second-degree type I SA block or SA
Wenckebach should always be suspected when there is
group beating. In this group beating, some QRS com-
Figure 12.5: Sinus Pause. A long pause of more than 3 seconds is terminated by a junctional escape complex
(arrow). A long pause is usually due to sinus arrest. It is also called sinus pause.
plexes are clustered together because they are separated
by pauses representing sinus impulses not conducted
to the atria. Group beating is commonly seen in type I
block because this type of block has a tendency to be
repetitive. In SA Wenckebach, there is gradual delay in
conduction between the sinus node and the atrium.
Because sinus node to atrial interval cannot be meas-
ured, only the gradual shortening of the P-P or R-R in-
tervals before the pause may be the only indication that
SA Wenckebach is present (Fig. 12.9).
Thus, group beating with shortening of the P-P inter-
val before the pause should always raise the possibility
of SA Wenckebach as shown in Figures 12.8B, 12.9, and
12.10. In Figure 12.9, there is group beatings labeled #1
to #3. The shortening of the R-R (or P-P) intervals
before the pause is better appreciated by the distances
between the arrows at the bottom of the tracing, which
represent the R-R intervals.
Tachycardia-Bradycardia Syndrome
Tachycardia-bradycardia syndrome: When the si-
nus node fails to function as the pacemaker of the
heart, ectopic rhythms come to the rescue, which en-
hances the vulnerability of the patient to develop atrial
arrhythmias, including atrial tachycardia, atrial flutter,
or atrial fibrillation. These arrhythmias are usually
sustained and most often become the dominant
rhythm. During tachycardia or during atrial flutter or
fibrillation, the presence of sinus node dysfunction is
not obvious until the atrial arrhythmia terminates
spontaneously. If there is sick sinus syndrome, the
sinus node is unable to take over the pacemaking func-
tion of the heart and the long pause that follows is a
frequent cause of syncope in tachycardia-bradycardia
syndrome (Figs. 12.11 and 12.12).
Chronic Atrial Fibrillation
Chronic atrial fibrillation: Atrial fibrillation is not an
uncommon sequela of sick sinus syndrome. Before the
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Sinus Node Dysfunction 151

840 ms 840 ms 840 ms 840 ms 840 ms

Figure 12.6: Sinoatrial Exit Block. The rhythm strips are continuous. A long period of asystole labeled
distance A is equal to distance B. A contains three P-QRS-T complexes that are missing, which are marked by the red
hearts.The long pause is due to sinoatrial exit block. ms, milliseconds.

2080 ms 2080 ms 2080 ms

1040 ms 1040 ms 1040 ms 1040 ms 1040 ms 1040 ms

Figure 12.7: Sinoatrial Exit Block. In sinoatrial exit block, the P-P intervals are fixed.
Note that the longer P-P intervals measure 2,080 milliseconds and are equal to two shorter
P-P intervals, which measure 1,040 milliseconds. This is due to SA exit block. Each red heart
represents an entire P-QRS-T complex that is missing. ms, milliseconds.

Figure 12.8: Sinoatrial (SA) Exit

A. Normal Baseline: Block. (A) Normal sinus rhythm.
(B) Type I second degree SA Wenckebach.
Shortening of the P-P intervals before a
780 ms 680 ms 1140 ms
pause is the hallmark of SA Wenckebach.
P-P interval #2 is shorter than P-P inter-
B. 2 Type I or SA #1 #2 #3 val #1. The pause is represented by P-P
Wenckebach interval #3. (C) Type II second-degree
P-P interval shortens before the pause SA exit block. An entire P-QRS-T
complex represented by the red heart is
missing. This long P-P interval is equiva-
1280 ms 1280 ms 1280 ms lent to two P-P intervals straddling a
sinus complex. (D) This rhythm is con-
sistent with third-degree SA exit block,
C. 2 Type II SA
Exit Block although this cannot be distinguished
P-P intervals are fixed
from sinus arrest. The sinus impulse
cannot conduct to the atria hence sinus
P waves are not present.
D. Probable 3 SA
Exit Block or
Sinus Arrest
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152 Chapter 12

#1 #2 #3

710 680 1170 700 670 1150

Figure 12.9: Sinoatrial (SA) Wenckebach. The rhythm strips were recorded in lead II. SA
Wenckebach should always be suspected when there is group beating labeled #1 to #3. These QRS com-
plexes are grouped together because they are separated by pauses, which represent the sinus impulses
that are not conducted to the atrium. Note also that there is gradual shortening of the R-R (or P-P) intervals
before the pause as shown by the distances between the arrows. This is the hallmark of SA Wenckebach.
The numbers between the arrows (between the QRS complexes) are in milliseconds.

Figure 12.10: Group Beating in Sinoatrial (SA) Wenckebach. Lead II rhythm strip showing group beating
similar to the electrocardiogram in Figure 12.9. There is also shortening of the R-R (or P-P) intervals before the long
pauses consistent with SA Wenckebach.

Figure 12.11: Tachycardia-Bradycardia Syndrome. The rhythm strips are continuous. Note that the atrial
tachycardia is paroxysmal with sudden onset and termination. When the tachycardia terminates abruptly, long
pauses follow, which are terminated by marked sinus bradycardia.
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Sinus Node Dysfunction 153

Figure 12.12: Prolonged Asystole as a Result of Tachycardia-Bradycardia Syndrome. The two

rhythm strips are simultaneous showing a supraventricular tachycardia followed by a long pause of more than
5 seconds before a junctional escape complex comes to the rescue.

era of cardiac pacemakers, atrial fibrillation may have

been the only spontaneous cure for patients with signifi-
cant bradycardia resulting from sinus node dysfunction.
Unfortunately, atrial fibrillation may be intermittent and
impermanent. When it terminates spontaneously, the
sinus node is unable to provide any rhythm and a long
asystole can occur (Figs. 12.13 and 12.14).
Patients with chronic atrial fibrillation frequently un-
dergo electrical cardioversion to convert the atrial fib-
rillation to normal sinus rhythm. After the atrial fibril-
lation is terminated by an electrical shock, the sinus
node is unable to provide a sinus impulse, thus a long
period of asystole may occur if the atrial fibrillation is
due to sick sinus syndrome. Sick sinus syndrome
should be suspected in patients with chronic atrial fib-
rillation when the ventricular rate is slow but are not
on AV nodal blocking agents because sick sinus syn-
drome is often due to degenerative disease that involves
not only the sinus node, but also the whole AV conduc-
tion system.
Escape Rhythms
Escape rhythms: When the rate of the sinus node be-
comes unusually slow, escape rhythms may originate
from the atria, AV junction, or ventricles. These cells
have intrinsically slower rates than the sinus node and
usually do not become manifest because they are depo-
larized by the propagated sinus impulse. When there is
sinus node dysfunction or when there is AV block (see
Chapter 8, Atrioventricular Block), these latent pace-
makers may become the dominant pacemaker of the
heart.
Atrial escape rhythm: The atrial impulse origi-
nates from cells in the atria usually at the area of the
coronary sinus and is followed by a narrow QRS
complex (Fig. 12.15).
AV junctional rhythm: The AV junction includes
the AV node down to the bifurcation of the bundle
of His. The escape impulse usually originates below

Figure 12.13: Sick Sinus Syndrome Manifesting as Atrial Fibrillation. Lead II rhythm strip showing
atrial fibrillation. Long pauses can occur when there is sick sinus syndrome because the sinus node is unable to
provide a sinus impulse when the atrial fibrillation terminates spontaneously. These long pauses can cause syncope
or sudden death.
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154 Chapter 12
Figure 12.14: Sick Sinus Syndrome and Atrial Fibrillation. Rhythm strip showing atrial fibrillation
followed by a long period of asystole of 5 seconds spontaneously terminated by a junctional escape complex.
the AV node at its junction with the bundle of His
and has a rate of 40 to 60 bpm 12.16).
Ventricular escape rhythm: Instead of the atria or
AV junction, the ventricles may be the origin of the
escape complex. A ventricular escape complex is
wide, measuring 0.12 seconds because it origi-
nates below the bifurcation of the bundle of His
(Fig. 12.17).
Junctional Escape Rhythms
AV junctional escape complex: AV junctional escape
rhythms are the most common escape rhythms when
there is bradycardia resulting from sinus node dysfunc-
tion or AV block (Fig. 12.18). The ectopic impulse may
or may not be associated with retrograde P waves.
When retrograde P waves are present, they may occur
before or after the QRS complex and are inverted in
leads II, III, and aVF (Fig. 12.19).
P waves before the QRS complex: Retrograde P
waves will occur in front of the QRS complex if con-
duction of the impulse to the atria is faster than con-
duction of the impulse to the ventricles. This type of
junctional escape rhythm may be difficult to differ-
entiate from an atrial escape complex. If the impulse
is junctional, the PR interval is usually short, meas-
uring 0.12 seconds, and the retrograde P waves are
usually narrow because the impulse originates from
the AV node, causing both atria to be activated
simultaneously.
No P waves: When P waves are absent, the im-
pulse may be blocked at the AV node or the retro-
grade P wave may be synchronous with the QRS
complex. This occurs when the speed of conduc-
tion of the impulse to the atria is the same as the
Figure 12.15: Atrial Escape Rhythm. Atrial escape complexes (arrows) can become the dominant pacemaker
when there is slowing of the sinus impulse.
speed of conduction of the impulse to the ventri-
cles (Fig. 12.18).
P waves after the QRS complex: The retrograde P
waves may occur after the QRS complex if conduc-
tion of the impulse to the ventricles is faster than
conduction of the impulse to the atria.
The 12-lead ECG of a patient with AV junctional escape
rhythm resulting from sinus node dysfunction (Fig.
12.20) and another patient with ventricular escape
rhythm also from sinus node dysfunction (Fig. 12.21)
are shown.
Wandering atrial pacemaker: Escape complexes may
originate from two or more locations in the atria and
compete with the sinus node as the pacemaker of the
heart (Fig. 12.22). Ectopic impulses from the AV junc-
tion may also compete as pacemaker as shown in Figure
12.23. In wandering atrial pacemaker, the ectopic atrial
impulses have the same rate as the sinus node (Figs.
12.22 and 12.23) and may even be late or slower (Fig.
12.24). Thus, the rhythm passively shifts from sinus
node to ectopic atrial. They should not be confused
with multifocal or chaotic atrial rhythm where the atrial
complexes are premature and anticipate the next sinus
impulse.
Accelerated rhythms: Very often, these escape
rhythms become accelerated and develop a rate that is
faster than their intrinsic rates. Thus, when the rate of
the AV junction is 40 to 60 bpm, the rhythm is called
accelerated junctional rhythm (Fig. 12.25); when the
ventricles exceed their intrinsic rate of 20 to 40 bpm,
the rhythm is called accelerated idioventricular rhythm
(Figs. 12.26 and 12.27).
Accelerated idioventricular rhythm: Two examples of
accelerated idioventricular rhythm are shown in Figures
12.26 and 12.27. Accelerated idioventricular rhythm is a
rhythm that is often confusing and difficult to recognize
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Figure 12.16: Atrioventricular (AV) Junctional Escape Complex. Arrow points to an AV junctional
escape complex. The escape complex terminates a long pause.

Figure 12.17: Ventricular Escape Rhythm. Rhythm strip showing ventricular escape complexes (stars) termi-
nating a sinus pause. The third complex (arrow) is a ventricular fusion complex.

Figure 12.18: Junctional Escape Rhythm. Lead II rhythm strip showing junctional rhythm with a rate of
46 bpm with narrow QRS complexes and no P waves because of sinus node dysfunction.

Figure 12.19: Junctional Escape Rhythm. Lead II rhythm strip showing junctional escape rhythm. The retro-
grade P waves are narrow and occur after (first arrow), within (second arrow), and before the QRS complexes (third,
fourth, and fifth arrows). The retrograde P wave in the second complex deforms the terminal portion of the QRS
complex and can be mistaken for an S wave.

Figure 12.20: Atrioventricular (AV) Junctional Rhythm. Twelve-lead electrocardiogram showing total
absence of sinus node activity. The rhythm is AV junctional with narrow QRS complexes.

155
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156 Chapter 12

Figure 12.21: Ventricular Escape Rhythm. Twelve-lead electrocardiogram showing ventricular escape
rhythm. The QRS complexes are wide with a regular rate of 34 bpm. There is no evidence of sinus node activity (no
P waves) in the whole tracing.

Figure 12.22: Wandering Atrial Pacemaker. The P waves have different morphologies and originate from
different locations from the atria. The rate is approximately 80 beats per minute.

Figure 12.23: Wandering Pacemaker. The morphology of the P waves is variable because the escape impulses
originate from different locations in the atria and atrioventricular junction.

Figure 12.24: Wandering Atrial Pacemaker. Lead II rhythm strip showing P waves with varying morpholo-
gies. The complexes originate from different foci in the atria and are late.
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Sinus Node Dysfunction 157

Figure 12.25: Accelerated Junctional Rhythm. Lead II rhythm strip showing accelerated AV junctional
rhythm, 73 bpm with retrograde P waves after the QRS complexes (arrows).

Figure 12.26: Accelerated Idioventricular Rhythm (AIVR). The ventricular rate is 70 bpm. The QRS com-
plexes are wide measuring 0.12 seconds, consistent with AIVR. The QRS complexes have right bundle branch
block configuration and no P waves are present.

Figure 12.27: Accelerated Idioventricular Rhythm (AIVR) with Ventriculoatrial Conduction. The
ventricular rate is 54 bpm with wide QRS complexes consistent with AIVR. The configuration of the QRS complexes
is different when compared with that shown in Figure 12.26. In addition, there is ventriculoatrial conduction with
retrograde P waves after the QRS complexes (arrows).
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158 Chapter 12

4 seconds

Figure 12.28: Hypersensitive Carotid Sinus. Sinus dysfunction is often due to vagal
influences, including the presence of hypersensitive carotid sinus. When the carotid sinus is
stimulated as shown, the pauses that follow generally do not last more than 3 seconds
because they are normally terminated by escape complexes. Pauses of 3 seconds that oc-
cur spontaneously or during carotid sinus stimulation are abnormal, as in this example, indi-
cating the presence of hypersensitive carotid sinus without adequate escape complexes.

because the configuration of the QRS complexes varies gests that a hypersensitive carotid sinus is present
depending on the origin of the ectopic impulse. (Fig. 12.28).
Hyperkalemia: Hyperkalemia can also suppress
sinus node function resulting in junctional escape
Reversible Causes of Sinus Dysfunction rhythm as shown in Figure 12.29.

Extrinsic causes of sinus node dysfunction: Exam-

ples of sinus node dysfunction not from sick sinus syn-
drome are shown in Figs. 12.28 and 12.29.
Hypersensitive carotid sinus: Extrinsic or re-
versible causes of sinus node dysfunction include
autonomic reflexes as well as the presence of hyper-
sensitive carotid sinus. During carotid sinus stimu-
lation, a long period of asystole can occur. In normal
individuals, the pause should not exceed 3 seconds.
A pause of 3 seconds or more is abnormal and sug-
Common Mistakes in Sinus
Node Dysfunction
Blocked premature atrial complex (PAC): One of the
most common errors in the diagnosis of sinus node dys-
function is the presence of blocked PACs. When a PAC is
blocked, a pause follows because the atrial impulse is not
conducted to the ventricles and is not followed by a QRS
complex (see Chapter 13, Premature Supraventricular

Figure 12.29: Hyperkalemia. In hyperkalemia, P waves may disappear because of sinus suppression or
marked slowing in the conduction of the sinus impulse in the atria. Impairment in sinus node function associated
with hyperkalemia is reversible.
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Sinus Node Dysfunction 159

Figure 12.30: Blocked Premature Atrial Complexes (PACs). The long R-R intervals are not due to sinus
pauses but are due to blocked PACs. The first PAC (first arrow) is conducted with aberration. The last two PACs (mid-
dle and last arrows) are blocked. The PACs can be identified by the presence of P waves riding on top of the T wave
of the previous complex (compare the T wave with arrows and those without). Thus, the T wave with a PAC looks
taller when compared to the other T waves without PACs.

Complexes). The ectopic P wave is visible because it usu-
ally deforms the ST segment or T wave before the pause.
Before sinus node dysfunction is considered as the cause
of a sudden pause, a blocked PAC should always be ex-
cluded first because this is the most common cause of
sudden lengthening of the R-R interval as shown in sev-
eral examples (Figs. 12.3012.33).
Blocked PACs in bigeminy mistaken for sinus
bradycardia: Blocked PACs occurring in bigeminy
can be mistaken for sinus bradycardia as shown in
Figure 12.34A, B. Figure 12.34A starts with normal si-
nus rhythm at 74 bpm. The third complex is a PAC
conducted aberrantly followed by normal sinus
rhythm and a succession of blocked PACs in bigeminy
(arrows). The 12-lead ECG in Figure 12.34B is from
the same patient showing a slow rhythm with a rate of
44 bpm. The rhythm is slow not because of sinus
bradycardia but because of blocked PACs in bigeminy.
The atrial rate, including the blocked PACs, is actually
double and is 88 beats per minute.
Sinus arrhythmia: Another common error that can
be confused with sinus node dysfunction is sinus ar-
rhythmia. In sinus arrhythmia, the sinus rate is irregu-
lar. Although sinus arrhythmia is a normal finding, the
long P-P (or R-R) intervals can be easily mistaken for
sinus pauses (Fig. 12.35). Sinus arrhythmia is more
frequent and much more pronounced in infants and in
young children.
In sinus arrhythmia, the difference between the
longest and shortest P-P interval should be 10%
or 0.12 seconds.
All P waves originate from the sinus node. Thus, the
P waves are generally uniform in configuration and
the P-R interval is usually the same throughout
(Fig. 12.35). In Figure 12.36, the rhythm is not sinus
arrhythmia because the P waves have different mor-
phologies; thus, not all P waves are of sinus node
origin. This is due to wandering atrial pacemaker
and not sinus arrhythmia.
The shortening and lengthening of the P-P intervals
are usually cyclic because sinus arrhythmia is com-
monly respiratory related, causing the intervals to
shorten during inspiration and widen during expira-
tion. This changing P-P interval is due to vagal effects.
During inspiration, vagal influence is diminished
causing the rate to increase. During expiration, the
rate decreases as vagal influence is enhanced. Sinus ar-
rhythmia may not be respiratory related when there is
enhanced vagal tone, as would occur in patients who
are taking digitalis.
Permanent Pacemakers and
Sinus Node Dysfunction
Permanent pacemakers and sinus node dysfunc-
tion: The following are the indications for implanta-
tion of permanent pacemakers in patients with sinus
node dysfunction according to the ACC/AHA/NASPE
guidelines (Fig. 12.38).
ECG Findings
The ECG findings of sinus node dysfunction are summarized
diagrammatically in figure 12.37 and include the following:
1. Inappropriate sinus bradycardia
2. Sinoatrial block, sinus arrest, and sinus pauses

Figure 12.31: Blocked Premature Atrial Complexes (PACs). Note that whenever there is a long pause, the
ST segment of the previous complex is deformed by a dimple marked by the arrows. The dimples represent
nonconducted PACs. Note that there are no dimples in complexes without pauses.
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160 Chapter 12

Figure 12.32: Blocked Premature Atrial Complexes (PACs). The arrow points to a nonconducted PAC, the
most common cause of sudden lengthening of the P-P and R-R intervals.

Figure 12.33: Blocked Premature Atrial Complexes (PACs) Resembling Sinus Pauses. The arrows
point to nonconducted PACs superimposed on the T wave of the previous complex. The tall QRS complex is a prema-
ture ventricular impulse.

PAC Conducted Aberrantly Blocked PACs in Bigeminy

Figure 12.34: Blocked
Premature Atrial Complexes A.
(PACs) in Bigeminy Resembling
Sinus Bradycardia. (A) The
rhythm is normal sinus at 74 beats
per minute (first two sinus complexes
on the left). The first arrow shows a
Blocked PACs in Bigeminy
PAC that is conducted with
B.
aberration. The subsequent PACs are
blocked PACs occurring in bigeminy
(arrows). (B) Twelve-lead electrocar-
diogram obtained from the same pa-
tient showing blocked PACs (arrows)
in bigeminy. The slow heart rate can
be mistaken for sinus bradycardia.

Figure 12.35: Sinus Arrhythmia. The variation in P-P interval is due to sinus arrhythmia. In sinus arrhythmia,
the longest P-P interval should measure 0.12 seconds when compared with the shortest P-P interval. The longer
intervals may be mistaken for sinus arrest or sinus pause.
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Sinus Node Dysfunction 161

Figure 12.36: This is not Sinus Arrhythmia. The rhythm strip shows irregular R-R intervals; however, the
P waves (arrows) are not the same throughout because some are ectopic in origin. The rhythm is wandering atrial
pacemaker. In sinus arrhythmia, all P waves should originate from the sinus node and should have the same config-
uration throughout.

3. Tachycardia-bradycardia syndrome
4. Chronic atrial fibrillation
5. Escape rhythms from the atria, AV junction, or ventricles
Mechanism
The sinus node is the pacemaker of the heart and is the ori-
gin of the sinus impulse. Because the electrical impulse from
the sinus node is not of sufficient magnitude, it does not
cause any deflection in the surface ECG. The sinus impulse is
recognized only when it has spread to the atria and is in-
scribed as a P wave in the ECG. The anatomy and electro-
physiology of the sinus node and normal sinus rhythm has
already been discussed elsewhere (see Chapter 1, Basic
Anatomy and Electrophysiology).
When the sinus node fails to function as the pacemaker of
the heart, supraventricular or ventricular escape impulses
usually come to the rescue. If there are no escape impulses,
the ultimate expression of total sinus failure is complete ab-
sence of P waves in the ECG, which is represented by a long

Summary of ECG Findings in Sick Sinus Syndrome Figure 12.37: Diagrammatic Representa-
tion of the Different Arrhythmias
Associated with Sick Sinus Syndrome. The
arrows point to sinus P waves and the red hearts
1 represent sinus impulses that are blocked.
Inappropriate Sinus Bradycardia

2
Sino-Atrial Exit Block

Sinus Arrest

Sinus Arrest or Sinus Pause

5
Junctional Escape Rhythm due to Complete SA Block or Sinus Arrest

6
Tachycardia-Bradycardia Syndrome

7
Chronic Atrial Fibrillation with Slow Ventricular Rate
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162 Chapter 12

Use of Permanent Pacemakers in Patients with

Sinus Node Dysfunction

Symptomatic Patient Asymptomatic Patient

Class I Class I

Sinus node dysfunction with documented symptomatic

bradycardia including frequent sinus pauses.
None
Symptomatic chronotropic incompetence.
Class IIa
Symptomatic sinus bradycardia that result from required drug
therapy for medical conditions.

Class IIa
None
Sinus node dysfunction with heart rate <40 bpm when a clear
association between symptoms of bradycardia and actual Class IIb
presence of bradycardia has not been documented.
None
Syncope of unexplained origin when clinically significant
abnormalities of sinus node function are discovered or
Class III
provoked in electrophysiological studies.
Class IIb
Asymptomatic sinus node dysfunction
In minimally symptomatic patients, chronic heart rate <40
bpm while awake.

Class III

Not indicated for sinus node dysfunction in patients with

symptoms suggestive of bradycardia have been clearly
documented to occur in the absence of bradycardia.

Sinus node dysfunction with symptomatic bradycardia due to

nonessential drug therapy.

Figure 12.38: Implantation of Permanent Pacemakers in Patients with Sinus Node Dysfunction
According to the American College of Cardiology/American Heart Association/Heart Rhythm
Society Guidelines. Class I: Condition in which there is evidence or agreement that a given procedure is use-
ful and effective. Class IIa: The weight of evidence is in favor of usefulness or efficacy of the procedure or
treatment. Class IIb: Efficacy of the procedure or treatment is less well established. Class III: The procedure or
treatment is not useful or effective and in some cases may be harmful. Note that in patients with sinus node dys-
function, implantation of a permanent pacemaker is generally reserved for patients who are symptomatic.

flat line without any electrical activity. Unless an escape
rhythm originating from the atria, AV junction, or ventricles
comes to the rescue, syncope or sudden death can occur.
Escape rhythms usually originate anywhere in the specialized
AV conduction system except the middle portion of the AV
node. These pacemakers are called latent pacemakers because
they have a slower rate than the sinus impulse. They do not
become manifest because they are normally discharged by
the propagated sinus impulse. However, when the sinus node
fails to function appropriately, these latent pacemakers may
take over and become the dominant pacemaker of the heart.
The intrinsic rate of these latent or subsidiary pacemakers
is slower than the intrinsic rate of the sinus node. For ex-
ample, impulses originating from the AV junction have a
rate of 40 to 60 bpm and impulses originating from the dis-
tal His-Purkinje system and ventricles have a rate of 20 to
40 bpm. The intrinsic rate of these ectopic impulses can
become accelerated by sympathetic and parasympathetic
influences. Thus, an AV junctional rhythm with a rate of
60 bpm is called accelerated junctional rhythm and a
ventricular rhythm with a rate 40 is called accelerated
idioventricular rhythm.
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Clinical Implications
Sick sinus syndrome refers to the presence of sinus node dys-
function associated with structural abnormalities in the
sinus node. It should not include extrinsic causes of sinus
dysfunction, such as those resulting from pharmacologic
agents that can suppress the SA node, hyperkalemia, neuro-
cardiogenic reflexes including vagally mediated syncope,
hypersensitive carotid sinus, increased intracranial pressure,
sleep apnea, or hypothyroidism and other physiologic or
functional changes that affect the sinus node, which are tran-
sient or reversible. Thus, the presence of sinus node dysfunc-
tion should always trigger a workup for reversible causes
before the diagnosis of sick sinus syndrome is suspected.
Inappropriate sinus bradycardia: The manifestations of
sick sinus syndrome may be very subtle and intermittent and
may be difficult to differentiate from reversible sinus dys-
function. Between normal sinus function and total sinus
node failure are varying gradations of sinus node dysfunc-
tion. One of the earliest manifestations is inappropriate sinus
bradycardia. This arrhythmia is often difficult to differentiate
from sinus bradycardia occurring in normal individuals, es-
pecially those who are athletic or well conditioned. When
there is inappropriate sinus bradycardia, the rate of the sinus
node is unusually slow and does not increase sufficiently
with exercise.
Chronotropic incompetence: Chronotropic incompe-
tence is failure of the sinus node to increase in rate during ex-
ercise. Most patients with chronotropic incompetence will
not be able to attain 80% of their maximum predicted heart
rate during exercise testing. The maximum (100%) predicted
heart rate is calculated by subtracting the patients age from
220. Thus, if the patient is 70 years of age, the maximum
heart rate that is expected during maximal exercise is ap-
proximately 150 bpm (220 70  150 bpm). If the patient
is unable to attain 80% of the predicted maximum heart
rate, which is 120 bpm (150  0.80  120), the patient has
chronotropic incompetence.
Other arrhythmias resulting in sinus node dysfunction in-
clude the following.
SA exit block: In SA exit block, the sinus node is able to
generate impulses, but some impulses are blocked as they
exit out to the surrounding atria. The main abnormality
in SA exit block is one of impulse conduction. If one im-
pulse is blocked, a whole P-QRS-T complex will be miss-
ing. The P-P interval can be measured if the pause is ter-
minated by another sinus impulse but not by an escape
rhythm. If the P-P interval of the long pauses is mathe-
matically related to the shorter P-P intervals, the diagno-
sis is SA exit block.
Sinus arrest: In sinus arrest, the sinus node is unable to
generate impulses intermittently; thus, the main abnor-
mality is one of impulse formation. Sudden long pauses
also occur, but these pauses are not mathematically re-
lated to the shorter P-P intervals; thus, the long P-P inter-
val is not exact multiples of the shorter P-P intervals.
Sinus Node Dysfunction 163
Sinus pause: Sinus pauses can be used interchangeably
with sinus arrest because long pauses are most commonly
the result of sinus arrest. In normal individuals, sinus
pauses are commonly present but are short and do not ex-
ceed 3 seconds. When sinus pauses are longer than 3 sec-
onds, sinus dysfunction should be suspected even if no
symptoms are present.
Tachycardia-bradycardia syndrome and chronic
atrial fibrillation: When the sinus node fails, sinus
rhythm is often replaced by atrial fibrillation or atrial
tachycardia. The atrial arrhythmia can further suppress
sinus function because the atrial impulses do not only ac-
tivate the atria, but can also penetrate and repeatedly de-
polarize the sinus node during atrial fibrillation or atrial
tachycardia. When the atrial arrhythmia terminates spon-
taneously, the tachycardia is often followed by a long
pause because sinus node function is suppressed. Unless
the pause is terminated by an escape rhythm, the patient
will become completely asystolic, resulting in syncope or
sudden death. This can also occur when a patient with si-
nus dysfunction presents with chronic atrial fibrillation
and is electrically cardioverted. After termination of the
atrial fibrillation, a long asystolic period terminated by es-
cape impulses usually occurs.
Escape rhythms originating from the atria, AV junc-
tion, or ventricles: These escape rhythms may become
manifest when the sinus node defaults as the pacemaker
of the heart or when there is complete AV block. These
escape rhythms may be enhanced by sympathetic or
parasympathetic influences and may become accelerated.
Although accelerated junctional and ventricular rhythms
may occur in normal healthy individuals as well as in pa-
tients with structural heart disease, these accelerated
rhythms may be a sign of sinus node dysfunction.
The presence of sinus dysfunction is usually diagnosed by
cardiac monitoring. The type of monitoring depends on the
frequency of symptoms.
Holter monitor: Ambulatory Holter recording for 24 to
48 hours may be sufficient for most patients with frequent
symptoms that occur almost on a daily basis. In other pa-
tients with intermittent symptoms, longer monitoring
may be necessary.
Event recorder: The use of an event recorder that lasts
30 to 60 days may be necessary if symptoms are infrequent.
Implantable loop recorder: The use of an implantable
monitoring device inserted subcutaneously may be neces-
sary if the patient continues to be symptomatic and other
monitoring techniques have not been useful. This is capa-
ble of monitoring the patient for 12 to 14 months. The
loop recorder can also correlate whether the symptoms
are related to other causes or other arrhythmias.
Other tests to identify the presence of sinus node dysfunction
may include the following.
Exercise testing: Exercise stress testing may confirm the
diagnosis of chronotropic incompetence, but is usually
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164 Chapter 12
not useful in the diagnosis of other arrhythmias resulting
from sinus node dysfunction.
Electrophysiologic testing: This is an invasive test in
which electrodes are introduced transvenously into the
heart. Sinus node function is evaluated by measuring si-
nus node recovery time. This is performed by rapid atrial
pacing resulting in overdrive suppression of the sinus
node. When atrial pacing is abruptly discontinued, sinoa-
trial recovery time is measured from the last paced beat to
the next spontaneously occurring sinus impulse, which is
prolonged when there is sick sinus syndrome. The sensi-
tivity of electrophysiologic testing in the diagnosis of
bradyarrhythmias is generally low and is not routinely
recommended. This is more commonly used to exclude
ventricular arrhythmias in patients with coronary disease,
especially when there is history of syncope.
Sick sinus syndrome may be due to ischemia, inflammation,
infection including Lyme disease, rheumatic heart disease,
pericarditis, collagen disease, muscular dystrophy, infiltrative
diseases such as amyloid, sarcoid, hemochromatosis, hy-
pothyroidism, and vascular diseases due to ischemia or my-
ocardial infarction. It also includes sclerosis and other degen-
erative changes that involve not only the sinus node but the
whole AV conduction system.
Sick sinus syndrome may manifest abruptly with frank syn-
cope or sudden death. It can also occur more insidiously and
may remain asymptomatic for several years before it be-
comes fully manifests. Thus, it may be difficult to differenti-
ate sick sinus syndrome from reversible causes of sinus node
dysfunction.
Among the more common conditions that can be mistaken
for sinus node dysfunction are blocked PACs and sinus
arrhythmia.
Blocked PACs: When a premature atrial complex or PAC
occurs too prematurely, before the AV node or the rest of
the conduction system has fully recovered from the previ-
ous impulse, the PAC can be blocked at the AV node re-
sulting in premature ectopic P wave that is not followed
by a QRS complex. This is usually identified by the pres-
ence of nonconducted P wave superimposed on the T
wave of the previous complex. Nonconducted PACs and
not sinus pauses are the most common causes of sudden
lengthening of the P-P or R-R intervals. Nonconducted
PACs should be recognized because they are benign and
do not have the same prognosis as patients with sinus
node dysfunction. The pause caused by the noncon-
ducted PAC is not an indication for pacemaker therapy.
Sinus arrhythmia: Sinus arrhythmia is present when the
difference between the shortest and longest P-P interval is
10% or 0.12 seconds (120 milliseconds). Sinus arrhyth-
mia is a normal finding; however, the irregularity in the
heart rate can be mistaken for sinus pauses, especially
when there is marked variability in the R-R (or P-P) in-
tervals. The pause resulting from sinus arrhythmia is not
an indication for pacemaker therapy.
n Respiratory sinus arrhythmia: Sinus arrhythmia is
usually cyclic because it is respiratory related, result-
ing in increase in sinus rate with inspiration and de-
crease in rate with expiration. This has been ascribed
to reduction of vagal inhibition during inspiration, re-
sulting in shortening of the P-P and R-R intervals. The
marked variability in the sinus rate is more pro-
nounced in infants and young children.
n Nonrespiratory: Sinus arrhythmia may be nonrespi-
ratory related as would occur with digitalis therapy.
n Absence of sinus arrhythmia: Absence of heart rate
variability is more common in the elderly and in pa-
tients with diabetic neuropathy, which increases the
risk of cardiovascular events. Thus, absence of sinus
rate variability is often used as a marker for increased
risk of sudden cardiovascular death similar to patients
with low ejection fraction or nonsustained ventricular
arrhythmias after acute myocardial infarction or in
patients with cardiomyopathy and poor left ventricu-
lar systolic function.
Hypersensitive carotid sinus syndrome: Hypersensitive
carotid sinus syndrome should always be excluded in a pa-
tient with history of syncope who is suspected to have sinus
node dysfunction as the cause of the syncope. The symptoms
are often precipitated by head turning. The diagnosis of hy-
persensitive carotid sinus can be confirmed by carotid sinus
pressure while a rhythm strip is being recorded (see tech-
nique of performing carotid sinus pressure in Chapter 16,
Supraventricular Tachycardia due to Reentry). A pause that
exceeds 3 seconds during carotid stimulation is considered
abnormal.
Treatment
The presence of sinus dysfunction does not always indicate
sick sinus syndrome. Extrinsic causes of sinus dysfunction
are often reversible and should always be excluded. If sinus
dysfunction is due to extrinsic causes such as hypothy-
roidism or sleep apnea, treatment of the hypothyroid state or
the sleep apnea may not only prevent or delay progression of
sinus node dysfunction, but may be able to reverse the
process. Medications that can cause slowing of sinus rhythm
such as beta blockers, non-dihydropyridine calcium channel
blockers, rauwolfia alkaloids, digitalis, and antiarrhythmic
and antipsychotic agents should be eliminated. Thus, treat-
ment should be directed to the underlying condition, which
is often successful in reversing the arrhythmia.
In patients with sinus bradycardia, sinus pauses, or supraven-
tricular and ventricular rhythms with rates 50 bpm who
remain asymptomatic, no therapy is indicated other than to
identify and correct the cause of the bradycardia. Although
sinus pauses of 3 or more seconds is considered pathologic, it
does not necessarily imply that a permanent pacemaker
should be implanted if the patient is completely asympto-
matic.
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When prolonged asystole occurs during cardiac monitoring
and the patient is still conscious, forceful coughing should be
instituted immediately. Forceful coughing is commonly used
to terminate bradyarrhythmias in patients undergoing coro-
nary angiography but is seldom tried in other clinical settings.
Because it needs the cooperation of a conscious patient, it
should be tried as early as possible. Cough may be able to
maintain the level of consciousness for 90 seconds and can
serve as a self-administered cardiopulmonary resuscitation.
When there is symptomatic bradyarrhythmia because of
sinus dysfunction, atropine is the initial drug of choice.
Atropine is given intravenously with an initial dose of 0.5 mg.
The dose can be repeated every 3 to 5 minutes until a total
dose of 0.04 mg/kg or approximately 3 mg is given within
2 to 3 hours. This dose will result in full vagal blockade. If the
bradycardia remains persistent in spite of atropine, transcu-
taneous pacing should be instituted. If a transcutaneous
pacemaker is not effective, is not tolerable, or is not available,
sympathetic agents such as epinephrine, dopamine, isopro-
terenol, or dobutamine may be given until a temporary
transvenous pacemaker can be inserted. The treatment of
symptomatic bradycardia is discussed in more detail in
Chapter 8, Atrioventricular Block.
The use of permanent pacemakers is the only effective treat-
ment available but is usually reserved for symptomatic pa-
tients with sick sinus syndrome. The symptoms should be re-
lated to the sinus node dysfunction before a permanent
pacemaker is inserted. In patients with the tachycardia-
bradycardia syndrome, insertion of a permanent pacemaker
is the only therapy that is appropriate, because there is gener-
ally no effective therapy for bradycardia. Furthermore, phar-
macologic treatment to control tachycardia or to control the
ventricular rate in atrial fibrillation will result in further de-
pression of the sinus node, in turn resulting in more pro-
nounced bradycardia when the patient converts to normal si-
nus rhythm. The indications for insertion of permanent
pacemakers in patients with sinus node dysfunction accord-
ing to the ACC/AHA/HRS guidelines on permanent pace-
makers are summarized in Figure 12.38.
Sick sinus syndrome from idiopathic degenerative disease is
usually progressive and may involve not only the sinus node,
but also the whole conduction system. Thus, atrial pacing
combined with ventricular pacing should be considered in
these patients. When AV conduction is intact, a single-channel
AAI pacemaker may be sufficient. Dual-chamber programma-
ble pacemaker with automatic mode switching from AAI to
DDD may be more appropriate in anticipation of AV block or
atrial fibrillation that often develops in patients with sick sinus
syndrome (see Chapter 26, The ECG of Cardiac Pacemakers).
The use of dual-chamber pacemakers compared with single-
chamber VVI devices may diminish the incidence of atrial
fibrillation in patients with sick sinus syndrome. Mode
switching pacemaker, capable of automatically switching
from DDD to VVI, may be advantageous in patients with in-
termittent atrial fibrillation.
Sinus Node Dysfunction 165
Anticoagulation should be given to patients with chronic
atrial fibrillation to prevent thromboembolism. This is one
of the common causes of death in patients with sick sinus
syndrome manifesting with chronic atrial fibrillation (see
Chapter 19, Atrial Fibrillation).
In patients with sinus node dysfunction who are completely
asymptomatic, there are no clear-cut indications for insertion
of a permanent pacemaker according to the ACC/AHA/HRS
guidelines.
Although there is no effective chronic oral therapy for brady-
cardia associated with sick sinus syndrome, some patients
with sinus pauses 2.5 seconds who are symptomatic but re-
fuse permanent pacemaker insertion, slow-release theo-
phylline, 200 to 400 mg daily given in two divided doses, may
be tried. This is based on the observation that sick sinus syn-
drome is associated with increased sensitivity to adenosine.
Thus, theophylline, which is the antidote to adenosine, may
be able to reverse the bradycardia resulting from sinus
pauses. Hydralazine in small doses of 15 to 100 mg daily in
divided doses has also been tried with varying results.
Prognosis
When sinus dysfunction is due to isolated degenerative dis-
ease of the conduction system, the prognosis in these pa-
tients with sick sinus syndrome who receive permanent pace-
makers is good and is similar to patients in the same age
group without sick sinus syndrome.
The prognosis of other patients depends on the underlying
disease causing the sick sinus syndrome.
Suggested Readings
2005 American Heart Association guidelines for cardiopul-
monary resuscitation and emergency cardiovascular care:
Part 7.3, Management of symptomatic bradycardia and
tachycardia. Circulation. 2005;112:6777.
Belic N, Talano JV. Current concepts in sick sinus syndrome II.
ECG manifestation and diagnostic and therapeutic ap-
proaches. Arch Intern Med. 1985;145:722726.
Blaufuss AH, Brown DC, Jackson B, et al. Does coughing pro-
duce cardiac output during cardiac arrest? [abstract] Circu-
lation. 1978;5556 (Suppl III):III-68.
Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006
key data elements and definitions for electrophysiology stud-
ies and procedures: a report of the American College of
Cardiology/American Heart Association Task Force on Clin-
ical Data Standards (ACC/AHA/HRS Writing Committee to
Develop Data Standards on Electrophysiology. J Am Coll
Cardiol. 2006;48:23602396.
Criley JM, Blaufuss AH, Kissel GL. Cough-induced cardiac
compression. JAMA. 1976;236:12461250.
Ferrer MI. The Sick Sinus Syndrome. Mount Kisco, NY: Futura
Publishing Company; 1974:7122.
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166 Chapter 12
Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a Report of the American College of Cardiology/
American Heart Association Task Force on Practice Guide-
lines (Writing Committee to Revise the ACC/AHA/NASPE
2002 Guideline Update for Implantation of Cardiac Pace-
makers and Antiarrhythmia Devices). Circulation. 2008;117:
e350e408.
Lamas GA, Lee KL, Sweeney MO, et al. Ventricular pacing or
dual-chamber pacing for sinus-node dysfunction. N Engl J
Med. 2002;346:18541862.
Mangrum JM, DiMarco JP. The evaluation and management of
bradycardia. N Engl J Med. 2000;342:703709.
Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treat-
ment. In: Libby P, Bonow RO, Mann DL, et al. eds. Braun-
walds Heart Disease, A Textbook of Cardiovascular Medicine.
7th ed. Philadelphia: Elsevier Saunders; 2005:803810.
Saito D, Matsubara K, Yamanari H, et al. Effects of oral theo-
phylline on sick sinus syndrome. J Am Coll Cardiol. 1993;21:
11991204.
Strickberger SA, Benson W, Biaggioni I, et al. AHA/ACCF scien-
tific statement on the evaluation of syncope. J Am Coll Car-
diol. 2006;47:473484.
Vijayaraman P, Ellenbogen KA. Bradyarrhythmias and pace-
makers. In: Fuster V, Alexander RW, ORourke RA, eds.
Hursts The Heart. 11th ed. New York: McGraw-Hill Medical
Publishing Division; 2004:893907.
Weiss AT, Rod JL, Lewis BS. Hydralazine in the management of
symptomatic sinus bradycardia. Eur J Cardiol. 1981;12:261.
Wolbrette DL, Naccarelli GV. Bradycardias: sinus nodal dys-
function and atrioventricular conduction disturbances.
In: Topol EJ, ed. Textbook of Cardiovascular Medicine. 2nd
ed. Philadelphia: Lippincott Williams and Wilkins; 2002:
13851402.
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Premature Supraventricular
Complexes
Premature Atrial Complex
Ectopic impulse: Any impulse that does not originate
from the sinus node is an ectopic impulse. The ectopic
impulse may be supraventricular or ventricular in origin.
Supraventricular impulse: The impulse is supra-
ventricular if it originates from the atria or atri-
oventricular (AV) junction or anywhere above the
bifurcation of the bundle of His (Fig. 13.1).
Supraventricular impulses have narrow QRS com-
plexes because they follow the normal AV conduction
system and activate both ventricles synchronously.
Ventricular impulse: The impulse is ventricular if
it originates in the ventricles or anywhere below the
bifurcation of the bundle of His. The ventricular
impulse has wide QRS complex because the impulse
does not follow the normal AV conduction system.
It activates the ventricles sequentially by spreading
from one ventricle to the other by muscle cell
to muscle cell conduction. Ventricular complexes
will be further discussed in Chapter 21, Ventricular
Arrhythmias.
Supraventricular complexes may be premature or they
may be late.
Premature supraventricular complex: The
supraventricular complex is premature if it occurs
Sinus node
Atria
Atrial
Supraventricular
Impulses
AV node
Junctional
Bifurcation of the
Bundle of His
Ventricular
Ventricles Impulses
13
earlier than the next expected normal sinus impulse
(Fig. 13.2A). The premature supraventricular im-
pulse may originate from the atria or AV junction.
n Premature atrial complex: An early impulse
originating from the atria is called a premature
atrial complex (PAC).
n Premature junctional complex: An early im-
pulse originating from the AV junction is called a
premature junctional complex (PJC).
Late or escape supraventricular complex: The
supraventricular impulse is late if it occurs later
than the next expected normal sinus impulse (Fig.
13.2B). Similar to premature complexes, late com-
plexes may originate from the atria or AV junction.
Late impulses are also called escape complexes. Late
or escape complexes were previously discussed in
Chapter 12, Sinus Node Dysfunction.
Premature atrial complex: A PAC is easy to recog-
nize because the impulse is premature and is followed
by a pause.
Typical presentation: The typical presentation of
a PAC is shown in Figure 13.2A. Because the PAC
originates from the atria, the atria are always acti-
vated earlier than the ventricles; thus, the P wave al-
ways precedes the QRS complex. The P wave is not
only premature, but also looks different in size and
shape compared with a normal sinus P wave. The
Figure 13.1: Ectopic Impulses.
Ectopic impulses may be supraventricular
or ventricular in origin. Supraventricular
impulses originate anywhere above the
bifurcation of the bundle of His and could
be atrial or atrioventricular junctional.
Ventricular impulses originate from the
ventricles or anywhere below the bifurca-
tion of the bundle of His. The stars repre-
sent the origin of the ectopic impulses.
167
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168 Chapter 13

Atria

A
Premature atrial complex

Ventricles
B
Late or escape atrial complex

Figure 13.2: Premature and Late Atrial Complexes. The diagram on the left
shows an impulse originating from the atria (star). This ectopic impulse may be pre-
mature or late. A premature atrial impulse is shown in rhythm strip A. The atrial
impulse occurs earlier than the next normal sinus impulse.The premature P wave is
recognized as a notch superimposed on the down slope of the T wave of the previous
complex (arrow). This premature impulse is followed by a narrow QRS complex.The
lower rhythm strip B shows a late atrial complex (arrow). The atrial complex occurs
later than the next expected sinus impulse with a P wave configuration that is differ-
ent from the sinus P waves. This late impulse is also called an escape atrial complex.

QRS complex is typically narrow similar to a nor-
mally conducted sinus impulse (Fig. 13.2A).
Other presentations:
n Blocked or nonconducted PAC: The PAC may
be completely blocked, meaning that the atrial
impulse may not be conducted to the ventricles.
n PAC conducted with prolonged PR interval:
The PAC may be conducted to the ventricles with
a prolonged PR interval.
n PAC conducted with aberration: The PAC may
be conducted to the ventricles with a wide QRS
complex and mistaken for PVC.
Blocked PAC: A premature atrial impulse may not be
conducted to the ventricles because of a refractory AV
node or His-Purkinje system. This usually occurs when
the PAC is too premature and the AV node or His-
Purkinje system has not fully recovered from the previ-
ous impulse. This is seen as a premature P wave with-
out a QRS complex (Fig. 13.3). The P wave may be
difficult to recognize if it is hidden in the T wave of the
previous complex or the P wave is flat or isoelectric and
is not visible in the lead used for recording.
PAC with prolonged PR interval: Instead of the pre-
mature P wave being completely blocked without a
QRS complex, the atrial impulse may be delayed at the
AV node resulting in a prolonged PR interval measur-
ing 0.20 seconds (Fig. 13.4).
PAC conducted with aberration: The premature
atrial impulse may be conducted normally across the
AV node and bundle of His, but may find one of the

Figure 13.3: Blocked PAC. The arrow points to a premature P wave without a QRS complex. This is an example of
a blocked or nonconducted PAC. The premature P wave can not conduct across the AV node because the AV node is
still refractory from the previous impulse. The premature P wave may not be apparent because it is hidden by the
T wave of the previous complex, thus the pause following the PAC may be mistaken for sinus arrest or sinoatrial block.
LWBK271-C13_167-179.qxd 29/1/09 9:52 pm Page 169 LWBK270-4119G-C02_073-110.qxd
Figure 13.4: Premature Atrial Complex (PAC) Conducted with a Prolonged PR Interval. The PAC
marked by the arrow, is conducted with a prolonged PR interval (bracket). The P wave is premature and has a
different configuration when compared to the normal sinus P waves. In spite of the prolonged PR interval, the
impulse is conducted normally to the ventricles resulting in a narrow QRS complex.
bundle branches still refractory from the previous im-
pulse. Thus, the PAC will be conducted across one bun-
dle branch (but not the other branch that is still refrac-
tory), resulting in a wide QRS complex. PACs that are
conducted with wide QRS complexes are aberrantly
conducted PACs. Aberrantly conducted PACs usually
have a right bundle branch block configuration be-
cause the right bundle branch has a longer refractory
period than the left bundle branch in most individuals.
Aberrantly conducted PACs are frequently mistaken
for PVCs because they have wide QRS complexes (Fig.
13.5).
PACs may also occur in bigeminy or in trigeminy (Figs.
13.613.9) or they may occur in pairs or couplets or in
short bursts of atrial tachycardia.
Atrial tachycardia: The rhythm is atrial tachycardia if
three or more PACs occur consecutively with a rate
100 beats per minute (bpm) (Fig. 13.10).
Multifocal atrial tachycardia: The tachycardia is
multifocal if the P waves have different morpholo-
gies (Fig. 13.11).
Premature Atrial Complex (PAC)
Figure 13.5:
Conducted with Aberration. The third QRS complex is pre-
mature and is wide and may be mistaken for a premature ven-
tricular contraction (PVC). Note, however, that there is an ectopic
P wave preceding the wide QRS complex (arrow), suggesting
that the wide QRS complex is a PAC, not a PVC. This type of PAC
with wide QRS complex is aberrantly conducted. Aberrantly
conducted PACs usually have right bundle branch block config-
uration and the QRS complexes are triphasic with rsR configu-
ration in V1 as shown.
Premature Supraventricular Complexes 169
Multifocal atrial rhythm: Multifocal atrial rhythm
is present if three or more consecutive PACS are
present with a rate 100 bpm (Fig. 13.12).
A single PAC can precipitate a run of atrial tachycardia,
atrial flutter, or atrial fibrillation when there is appro-
priate substrate for reentry (Fig. 13.13).
Compensatory pause: The pause after a PAC is usu-
ally not fully compensatory in contrast to the pause af-
ter a PVC, which is usually fully compensatory. A pause
is fully compensatory if the distance between two sinus
complexes straddling a PAC is the same as the distance
between two sinus complexes straddling a normal si-
nus impulse.
PAC: The PAC does not have a fully compensatory
pause because the PAC activates not only the atria,
but also resets the sinus node by discharging it ear-
lier than normal. Thus, the duration of two sinus cy-
cles straddling a PAC is shorter than the duration of
two similar sinus cycles straddling another sinus im-
pulse (Fig. 13.14).
PVC: The pause after a PVC is usually fully com-
pensatory because the PVC does not reset the si-
nus node (Fig. 13.15). Thus, the sinus node con-
tinues to discharge on time. However, if the PVC is
retrogradely conducted to the atria, it might reset
the sinus node and the pause may not be fully
compensatory.
Common Mistakes Associated
with PACs
PACs are commonly mistaken for other arrhythmias.
Blocked PACs may be mistaken for sinus arrest
or sinoatrial block: The pauses caused by blocked
PACs may be mistaken for sinus node dysfunction
and may result in an erroneous decision to insert a
temporary pacemaker (Fig. 13.16A, B).
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170 Chapter 13

Figure 13.6: Premature Atrial Complex (PAC) Occurring in Bigeminy. Every other complex is a PAC (arrows).

Figure 13.7: Premature Atrial Complex (PAC) in Trigeminy. Every third complex is a PAC.
The ectopic P waves are seen as small bumps deforming the T waves of the previous complexes
(arrows). The PACs are conducted normally and the QRS complexes are narrow.

Figure 13.8: Aberrantly Conducted Premature Atrial Complex (PAC) in Trigeminy. Every third
complex is a PAC. The ectopic P waves are marked by the arrows and are followed by wide QRS complexes that are
different from the sinus complexes. These PACs are aberrantly conducted.

Blocked PACs
Normally Aberrantly Normal Sinus
conducted PAC conducted PAC Rhythm

Figure 13.9: Normally Conducted, Aberrantly Conducted, and Blocked Prema-

ture Atrial Complex (PAC). The arrows point to the PACs. The first PAC is normally
conducted.The PR interval is short and the QRS complex is narrow. The second PAC is
conducted with aberration. An ectopic P wave is followed by a wide QRS complex. The third
and fourth PACs are blocked and are followed by pauses. The blocked PACs can be identified
by the presence of deformed T waves of the previous complexes. Note that the T waves of the
QRS complexes during normal sinus rhythm are flat (right side of the tracing), whereas the T
waves with blocked PACs are peaked and are followed by pauses.

Atrial tachycardia Atrial tachycardia

Figure 13.10: Atrial Tachycardia. Three or more consecutive premature atrial complexes
in a row is considered atrial tachycardia if the rate exceeds 100 beats per minute.
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Premature Supraventricular Complexes 171

Figure 13.11: Multifocal Atrial Tachycardia. When three or more consecutive multifocal premature atrial
complexes are present (arrows) with a rate 100 beats per minute, the rhythm is called multifocal atrial tachycardia.

Figure 13.12: Multifocal Atrial Rhythm or Chaotic Atrial Rhythm. The rhythm shows P waves with vary-
ing sizes and shapes (arrows) similar to the arrhythmia shown in Figure 13.11. The rate, however, is 100 beats per
minute and does not qualify as tachycardia. The arrhythmia is called multifocal atrial rhythm, chaotic atrial rhythm,
or simply sinus rhythm with multifocal premature atrial complexes.

Atrial fibrillation

Figure 13.13: Premature Atrial Complexes (PACs) Causing Atrial Fibrillation. A sin-
gle PAC (arrow) can precipitate atrial tachycardia, atrial flutter, or atrial fibrillation when there is
appropriate substrate for reentry.

A = 1640 ms B = 1800 ms

Figure 13.14: The Pause after a Premature Atrial Complex (PAC) is not
Fully Compensatory. The rhythm strip shows a PAC followed by a pause that is not
fully compensatory.The fourth P wave, marked by the star, is a PAC. Distance A, which in-
cludes two sinus impulses straddling the PAC is shorter than distance B, which includes
two sinus impulses straddling another sinus complex. ms, milliseconds.

A = 1360 ms B = 1360 ms A B

Figure 13.15: The Pause after a Premature Ventricular Contraction (PVC) is Usually
Fully Compensatory. The rhythm strip shows frequent PVCs.The pause after each PVC is
fully compensatory. Note that the distance between two sinus impulses straddling a PVC
(distance A) is the same as the distance between two sinus impulses straddling another sinus
impulse (distance B). ms, milliseconds.
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172 Chapter 13

Figure 13.16: Blocked Premature Atrial Complexes (PACs) Resembling Sinus Pauses. Rhythm strips
A and B are examples of blocked PACs (arrows). The premature P waves (arrows) are barely visible because they are
superimposed on the T wave of the previous complex. What is striking when PACs are blocked is the appearance of
sudden pauses. The pauses can be mistaken for sinus arrest or sinus pause.

Blocked PACs may also be mistaken for second-
degree AV block: The blocked PACs look like sinus P
waves that are not conducted and may be mistaken for
second-degree AV block. This may also result in an er-
roneous decision to insert a pacemaker (Fig. 13.17).
Aberrantly conducted PACs may be mistaken for
PVCs: Aberrantly conducted PACs have wide QRS
complexes that can be mistaken for PVCs (Fig. 13.18).
Blocked PACs in bigeminy mistaken for sinus
bradycardia: In Fig. 13.19A, the rhythm starts as nor-
mal sinus with a rate of 74 bpm. The third complex is a
PAC conducted aberrantly. This is followed by normal
sinus rhythm with a normally conducted QRS complex
and a succession of blocked PACs in bigeminy (ar-
rows), which can be mistaken for sinus bradycardia.
The 12-lead electrocardiogram (ECG) in Fig. 13.19B is
from the same patient showing a slow rhythm with a
rate of 44 bpm. The rhythm is slow not because of si-
nus bradycardia, but because of blocked PACs in
bigeminy. The atrial rate, including the blocked PACs,
is actually double and is 88 bpm.
den in the T wave of the previous complex or is isoelectric in
the lead used for monitoring.
2. The P wave is ectopic and therefore has a different contour
when compared with the sinus impulse.
3. The PR interval may be normal (0.12 seconds) or it may be
prolonged (0.20 seconds).
4. The P wave may be blocked and not followed by a QRS com-
plex; thus, only a pause may be present.
QRS complex
1. The QRS complex is narrow, similar to a normally conducted
sinus impulse.
2. The QRS complex may be wide when the impulse is con-
ducted to the ventricles aberrantly or there is preexistent
bundle branch block.
3. A QRS complex may not be present if the PAC is blocked.
Compensatory pause
The pause after the PAC is usually not fully compensatory.

ECG Findings of Premature Atrial Complexes Mechanism

P wave: The PAC may originate anywhere in the atria in-
P wave and PR interval
cluding veins draining into the atria such as the coronary
1. The P wave is premature and is inscribed before the QRS sinus, pulmonary veins, and vena cava. The impulse origi-
complex. The P wave may be difficult to recognize if it is hid- nates from cells that are capable of firing spontaneously. The

Basic P-P interval

Figure 13.17: Blocked Premature Atrial Complexes (PACs) Resembling Atrioven-

tricular (AV) Block. The PACs are marked by the arrows. The first PAC is conducted to the ven-
tricles.The second and third PACs are blocked. The nonconducted PACs may be mistaken for
sinus P waves and the rhythm mistaken for second-degree AV block.
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Premature Supraventricular Complexes 173

Figure 13.18: Premature Atrial Complex (PAC) Conducted with Aberration. The first PAC (star) is con-
ducted to the ventricles normally. The QRS complex is narrow, similar to a normally conducted sinus impulse.
Another PAC is marked with an arrow. This PAC is conducted with aberration. The QRS complex after the P wave is
wide and can be mistaken for premature ventricular contraction.

ectopic P wave has a different contour compared with the
normal sinus impulse and always precedes the QRS complex.
QRS complex: The impulse follows the normal AV conduc-
tion system, resulting in a narrow QRS complex similar to a
normally conducted sinus impulse. The premature atrial im-
pulse may be delayed or blocked on its way to the ventricles,
depending on the prematurity of the PAC and state of refrac-
toriness of the AV node and conducting system.
Blocked PAC: If the AV node or distal conduction system
is still refractory (has not fully recovered) from the previ-
ous impulse, the PAC will activate only the atria, but will
not be able to conduct to the ventricles resulting in a pre-
mature P wave without a QRS complex.
Aberrantly conducted: The PAC is followed by a wide
QRS complex and can be mistaken for PVC. When the
PAC is too premature, it may be able to conduct through
the AV node, but finds either the right or left bundle
branch still refractory from the previous impulse. If the
right bundle branch is still refractory, the premature atrial
impulse will reach the ventricles only through the left
bundle branch instead of both bundle branches, resulting
in a wide QRS complex.
Compensatory pause: The PAC activates not only the atria
but also resets the sinus node by discharging it prematurely.
Thus, the pause after a PAC is not fully compensatory. Occa-
sionally, however, the sinus node may be suppressed by the
PAC preventing it from recovering immediately. This may re-
sult in a pause that is fully compensatory, similar to a PVC, or
the pause may even be longer than a full compensatory
pause.

PAC Conducted Aberrantly Blocked PACs in Bigeminy Figure 13.19: Blocked Prema-
ture Atrial Complexes (PACs)
A.
in Bigeminy Resembling
Sinus Bradycardia. (A) The
rhythm is normal sinus at 74 bpm
(first two sinus complexes on the
left). The first arrow shows a PAC
Blocked PACs in Bigeminy that is conducted with aberration.
B. The subsequent PACs are blocked
PACs occurring in bigeminy
(arrows). (B) Twelve-lead
electrocardiogram obtained from
the same patient showing blocked
PACs (arrows) in bigeminy. The
slow heart rate can be mistaken for
sinus bradycardia.
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174 Chapter 13

Clinical Significance Premature Junctional Complex

PACs frequently occur in normal individuals as well as those
with structural heart disease. These extra heartbeats may Atrioventricular junction: The AV junction includes
cause symptoms of palpitations. Most PACs, however, do not the AV node down to the bifurcation of the bundle of
cause symptoms and most individuals are not aware that His. It is the center of the heart because it is located
they have premature atrial impulses. They may be detected midway between the atria and ventricles.
during routine ECG, which may be taken for reasons other
Atrioventricular node: The AV node can be divided
than palpitations.
into three distinct areas with different electrophysio-
PACs, especially when frequent, may be caused by excessive
logic properties. These include the upper, middle, and
coffee or tea, smoking, diet pills, thyroid hormones, digitalis, lower AV node (Fig. 13.20).
antiarrhythmic agents, isoproterenol, theophylline, and al-
Upper AV node: The upper portion or head of the
buterol. They can also occur in the presence of electrolyte
AV node is directly contiguous to the atria. This
abnormalities, congestive heart failure, coronary disease,
portion is called AN, or atrionodal region. It re-
valvular heart disease (especially mitral valve prolapse),
ceives impulses from the atria and relays it to the
cardiomyopathy and other noncardiac conditions such as
rest of the conduction system. This area of the AV
pulmonary diseases, infections, thyroid disorders, and other
node contains cells that are capable of firing spon-
metabolic abnormalities.
taneously.
PACs may be mistaken for PVCs when they are aberrantly
Middle AV node: The middle portion of the AV
conducted or sinus pauses when they are nonconducted.
node is also called the N (nodal) region. This is the
Blocked PACs is the most common cause of sudden length-
body or AV node proper. This portion of the AV
ening of the P-P or R-R interval and should always be sus-
node contains cells that conduct slowly and is re-
pected before sinus node dysfunction is considered.
sponsible for the delay in the spread of the atrial
Although single or repetitive PACs are benign, they may trig-
impulse to the ventricles. This portion of the AV
ger sustained arrhythmias (atrial tachycardia, atrial flutter, or node does not contain cells that are capable of fir-
atrial fibrillation) when there is appropriate substrate for reen- ing spontaneously and therefore can not initiate an
try. Similar to the ventricles, the atria have a vulnerable period ectopic impulse.
in which a premature atrial impulse can precipitate atrial fib-
Lower AV node: The tail or lower portion of the AV
rillation. This often occurs when the PAC is very premature
node is directly contiguous with the bundle of His
with coupling interval that is 50% of the basic P-P interval
and is called NH or nodo-His region. This portion
(P to PAC interval is 50% of the basic rhythm). Thus, over-
of the AV node contains cells with pacemaking
all treatment of atrial tachycardia, flutter, or fibrillation may
properties and is usually the site of origin of the
include suppression or elimination of ectopic atrial impulses.
junctional impulse.
The AV junction is the only pathway by which the sinus
Treatment impulse is conducted to the ventricles. The AV junction
Ectopic atrial impulses generally do not cause symptoms. If is also the origin of the junctional impulse.
the patient is symptomatic and the palpitations have been Any impulse originating from the AV node or bundle
identified as resulting from PACs, treatment usually involves of His is a junctional impulse.
correction of any underlying abnormality, electrolyte disor-
der, or any precipitating cause that can be identified such as
exposure to nicotine, caffeine, or any pharmacologic agent
that can cause the arrhythmia. Treatment also includes reas- Upper or AN Region
surance that the arrhythmia is benign. Pharmacologic therapy
Mid or N Region AV Node
is not necessary. When reassurance is not enough, especially if
the patient is symptomatic, beta blockers may be tried and if AV
Lower or NH Region Junction
contraindicated because of reactive airway disease, nondihy-
dropyridine calcium channel blockers (diltiazem or vera- Bundle of
His
pamil) may be used as alternative.

Prognosis
Single or repetitive atrial complexes are benign in patients
without cardiac disease. In patients with known cardiac dis-
ease, the prognosis depends on the nature of the cardiac ab-
normality and not the presence of atrial ectopy.
Figure 13.20: Diagrammatic Representation of the
Atrioventricular (AV) Junction. The AV junction includes
the AV node down to the bifurcation of the bundle of His. The
AV node consists of the upper (AN region), mid- or AV node
proper (N region), and lower AV node (nodo-His) region.
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Premature Supraventricular Complexes 175

Atria P P P Figure 13.21: Premature Junctional

A Complex (PJC). The different patterns of PJC
or or
PJC
Retrograde P wave is in front of the QRS complex (the
atria are activated before the ventricles). The PR interval
is usually short measuring <0.12 second and can be
Ventricles
mistaken for a Q wave although it can be longer if the
impulse is delayed on its way to the atria.
are shown. (A) Retrograde P wave is inscribed
before the QRS complex. (B) Retrograde P wave
is inscribed after the QRS complex. (C)
Retrograde P wave is synchronous with the QRS
complex or the impulse is blocked on its way to
the atria, but is normally conducted to the ven-
tricles.

Atria
B P P P

or or

Retrograde P wave follows the QRS complex (the

ventricles are activated before the atria). The retrograde
Ventricles P wave can be mistaken for an S wave or it may be further
away from the QRS complex.

Atria
C

No P wave. The atria and ventricles are activated

simultaneously and the retrograde P wave is buried within
Ventricles the QRS complex.

Atrial activation: An impulse originating from the
AV junction will activate the atria retrogradely from
below upward because the AV junction is located be-
low the atria. This causes the P wave to be inverted in
leads II, III, and aVF. Both left and right atria are acti-
vated synchronously, causing the P wave to be narrow.
Ventricular activation: Because the AV junction is
located above the ventricles, an impulse originating
from the AV junction will activate the ventricles an-
terogradely through the normal AV conduction sys-
tem, resulting in narrow QRS complexes similar to a
normally conducted sinus impulse.
ECG findings: A PJC can manifest in several different
patterns, depending on the speed of conduction of the
junctional impulse to the atria and to the ventricles.
Thus, the retrograde P wave may occur before or after
the QRS complex or it may occur synchronously with
the QRS complex.
Retrograde P wave before the QRS complex:
Retrograde P wave occurring in front of the QRS
complex suggests that the speed of conduction of
the junctional impulse to the atria is faster than the
speed of conduction of the impulse to the ventricles
(Fig. 13.21A).
Retrograde P wave after the QRS complex: Ret-
rograde P wave occurring after the QRS complex sug-
gests that the speed of conduction of the junctional
impulse to the ventricles is faster than the speed of
conduction of the impulse to the atria (Fig. 13.21B).
Retrograde P wave synchronous with the QRS
complex: When there is simultaneous activation of
the atria and ventricles, the retrograde P wave will
be superimposed on the QRS complex and will not
be visible. Only a QRS complex will be recorded
(Fig. 13.21C). The retrograde P wave may also be
absent if the junctional impulse is blocked at the AV
node on its way to the atria but is conducted nor-
mally to the ventricles.
Figure 13.21 shows the different patterns of premature
junctional impulse when recorded in lead II.
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176 Chapter 13
Figure 13.22: Premature Junctional Complex (PJC)
with a P Wave Before the QRS Complex. Lead II rhythm
strip showing a PJC. When an ectopic P wave precedes the QRS
complex, a PJC may be difficult to differentiate from a prema-
ture atrial complex (PAC). In PJC, the P wave is always retrograde
and inverted in leads II, III, and aVF, which is not always the case
if the ectopic impulse is a PAC. The PR interval is usually short
measuring 0.12 seconds, although it could be longer if the ret-
rograde impulse is delayed at the atrioventricular (AV) node.The
retrograde P wave is narrow because the AV node is located in-
feriorly, midway between the atria, thus both atria are activated
retrogradely simultaneously. An atrial impulse is wider, especial-
ly if it originates from the lateral border of either atrium because
the impulse has to activate the atria sequentially instead of
simultaneously.
Examples of single premature junctional complexes are
shown (Figs. 13.2213.24). When P waves are present,
the P waves are always retrograde and are inverted in
leads II, III, and aVF and can occur before or after the
QRS complex.
Accelerated Junctional Rhythm
Accelerated junctional rhythm: The AV junction
has an intrinsic rate of approximately 40 to 60 bpm.
If the rate is 61 to 100 bpm, accelerated junctional
rhythm is the preferred terminology (Figs. 13.25
13.28). This rhythm is also traditionally accepted as
junctional tachycardia even if the rate is 100 bpm be-
cause junctional rhythm with a rate that is 60 bpm is
well above the intrinsic rate of the AV junction. This
is further discussed in Chapter 17, Supraventricular
Tachycardia due to Altered Automaticity.
A summary of the different supraventricular com-
plexes is shown diagrammatically in Figure 13.29.
Figure 13.23: Premature Junctional Complex (PJC) with a P Wave After the QRS Complex. Lead II
rhythm strip showing a PJC (fourth complex). The premature impulse starts with a QRS complex followed by a retro-
grade P wave (arrow).
Summary of ECG Findings
P wave
1. When P waves are present, they are always retrograde and are
inverted in leads II, III, and aVF.
2. The retrograde P wave may occur before the QRS complex.
3. The retrograde P wave may occur after the QRS complex.
4. The P wave may be entirely absent; thus, only a premature
QRS complex is present.
QRS complex
1. The QRS complex is narrow, similar to a normally conducted
sinus impulse.
2. The QRS complex is wide if there is pre-existent bundle
branch block or the impulse is aberrantly conducted.
No P wave or QRS complex
A unique and unusual presentation of PJC is absence of P
wave or QRS complex and is thus concealed.
Mechanism
The AV junction includes the AV node and bundle of His. The
AV node consists of three areas with different electrophysio-
logic properties: the AN (atrionodal), N (nodal), and NH
(nodo-His) regions corresponding to the top, middle, and
caudal portions, respectively. A premature junctional im-
pulse may originate anywhere in the AV junction except the
middle portion of the AV node because this portion of the
AV node does not contain cells with pacemaking properties.
Junctional impulses usually originate from the NH region.
Because the AV junction lies midway between the atria and
ventricles, the atria are activated retrogradely from below up-
ward in the direction of 60 to 150. Thus the P waves are
inverted in leads II, III, and aVF and are upright in leads aVR
and aVL. The ventricles are activated anterogradely through
the bundle of His and normal intraventricular conduction
system. The QRS complexes are narrow, similar to a normally
conducted sinus impulse, but may be wide if there is preexis-
tent bundle branch block or if the impulse is conducted
aberrantly.
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Premature Supraventricular Complexes 177

Figure 13.24: Premature Junctional Complex (PJC) Without a P Wave. Lead II rhythm strip showing PJC
without a retrograde P wave. The P wave is buried within the QRS complex or the junctional impulse may have
been blocked retrogradely on its way to the atria. It is also possible that an ectopic P wave is present but the axis of
the P wave is isoelectric in this lead used for recording.

II

Figure 13.25: Accelerated Junctional Rhythm With P Waves Before the QRS Complexes. Lead II
rhythm strip showing accelerated junctional rhythm with retrograde P waves preceding the QRS complexes
(arrows) with very short PR intervals. The retrograde P waves can be mistaken for Q waves. Although the rate is
100 bpm, the rhythm is traditionally accepted as junctional tachycardia because it exceeds its intrinsic rate of
40 to 60 bpm.

Figure 13.26: Accelerated Junctional Rhythm With P Waves After the QRS Complexes. Lead II rhythm
strip showing accelerated junctional rhythm with retrograde P waves immediately after the QRS complexes (arrows).
The retrograde P wave can be mistaken for S waves. Note that the P waves are narrow.

II

Figure 13.27: Accelerated Junctional Rhythm Without P Waves. Retrograde P waves are not present.

II

Figure 13.28: Junctional Rhythm with Complete Atrioventricular (AV) Dissociation. The rhythm is
accelerated junctional rhythm, also called junctional tachycardia (rate 80 beats per minute) with complete AV disso-
ciation. Note that the QRS complexes are regular and are completely dissociated from the P waves (arrows). The
P waves are regular and are normal sinus in origin (P waves are upright in lead II).
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178 Chapter 13

Normal Sinus
Rhythm

Premature Atrial
Complex

PAC Conducted
with Aberration

Blocked PAC

Premature
Junctional
Complex

Premature
Junctional
Complex

Premature
Junctional
Complex

Atrial
Tachycardia
(Multifocal)

Figure 13.29: Premature Supraventricular Complexes. Diagram shows the differ-

ent types of supraventricular impulses. Arrows point to the ectopic supraventricular
complexes.

The retrograde P wave is usually narrow because both atria
are activated simultaneously. The P wave may occur before,
after, or within the QRS complex. The position of the P wave
in relation the QRS complex depends on the speed of con-
duction of the junctional impulse retrogradely to the atria
and anterogradely to the ventricles and not from the area of
origin of the impulse within the AV junction. There are other
possible ECG presentations of junctional rhythm. These in-
clude the following.
Complete AV dissociation: When there is junctional
rhythm, the junctional impulse may control the ventri-
cles, but not the atria. Thus, the P wave and the QRS com-
plex may be completely dissociated. When this occurs, the
atria are independently controlled by normal sinus
rhythm or by atrial fibrillation. The ventricles are inde-
pendently controlled by the junctional impulse.
Concealed junctional impulsesno P wave, no QRS
complex: It is possible that the junctional impulse is
blocked retrogradely on its way to the atria and antero-
gradely on its way to the ventricles; thus, no P wave or
QRS complex will be recorded. When this occurs, the PJC
is concealed or is nonconducted. The presence of a non-
conducted junctional impulse is not visible in the ECG,
but its presence can be inferred because it will affect the
next sinus impulse by rendering the AV node refractory.
This may result in varying degrees of pseudo-AV block.
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Thus, sudden and unexpected lengthening of the PR in-
terval or intermittent second-degree AV block may be the
only abnormality indicating the presence of concealed
junctional ectopic impulses.
Clinical Significance and Treatment
PJCs are much less common than PACs. Similar to PACs,
they can occur in normal individuals as well as those with
structural heart disease. Unlike PAC, in which the P wave al-
ways precedes the QRS complex, single or repetitive PJCs
have varying ECG presentations.
When the retrograde P wave is in front of the QRS complex,
a PJC may look like a PAC. The following findings suggest
that the ectopic impulse is AV junctional rather than atrial.
AV junctional impulses always conduct to the atria retro-
gradely, thus the P waves are always inverted in leads II,
III, and aVF. On the other hand, PACs may originate any-
where in the atria and may or may not be inverted in these
leads.
Junctional P waves are usually narrow because the AV
node lies in the lower mid-atria; thus, both atria are acti-
vated simultaneously.
The PR interval is usually short measuring 0.12 sec-
onds. The PR interval however may be longer if the junc-
tional impulse is delayed on its way to the atria.
Accelerated junctional rhythm is the preferred terminology if
the rate exceeds 60 bpm. This rhythm is also accepted as non-
paroxysmal junctional tachycardia because it is above the in-
trinsic rate of the AV junction, which is 40 to 60 bpm. Al-
though the tachycardia may be seen in perfectly normal
hearts, it is more commonly associated with inferior myocar-
dial infarction, rheumatic carditis, cardiac surgery, and digi-
talis toxicityespecially when there is associated hy-
pokalemia. Digitalis toxicity should be strongly considered
when there is atrial fibrillation with regularization of the R-R
Premature Supraventricular Complexes 179
interval in a patient who is taking digitalis. The arrhythmia
may also be an escape mechanism when there is primary si-
nus node dysfunction or when there is hyperkalemia. Thus,
the significance and treatment of nonparoxysmal junctional
tachycardia depends on the underlying condition, which may
be cardiac or noncardiac (see Nonparoxysmal Junctional
Tachycardia in Chapter 17, Supraventricular Tachycardia due
to Altered Automaticity).
Retrograde P waves occurring within or after the QRS com-
plex may cause cannon A waves in the neck because of si-
multaneous contraction of both atria and ventricles. Patients
therefore may complain of recurrent neck vein pulsations
rather than palpitations.
The clinical significance and treatment of single or repetitive
but nonsustained PJCs is the same as for PACs.
Prognosis
The prognosis of single and repetitive but nonsustained PJCs
is benign because these ectopic complexes are present in
structurally normal hearts.
Junctional ectopic rhythms, including accelerated junctional
rhythm, may be a sign of sinus node dysfunction or presence
of underlying heart disease or digitalis toxicity. The treat-
ment and prognosis of this rhythm depends on the underly-
ing cardiac condition.
Suggested Readings
Marriott HJL. Atrial arrhythmias. In: Practical Electrocardiogra-
phy. 5th ed. Baltimore: The William & Wilkins Co; 1972:
128152.
Wilkinson Jr DV. Supraventricular (atrial and junctional) pre-
mature complexes. In: Horowitz LN, ed. Current Management
of Arrhythmias. Philadelphia: BC Decker Inc; 1991;4750.
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14
Sinus Tachycardia
Electrocardiogram Findings
Sinus tachycardia: Sinus tachycardia refers to im-
pulses that originate from the sinus node with a rate
that exceeds 100 beats per minute (bpm). The 12-lead
electrocardiogram (ECG) is helpful in identifying the
presence of sinus tachycardia as well as excluding other
causes of tachycardia such as supraventricular tachy-
cardia (SVT), atrial flutter, and atrial fibrillation.
ECG findings: The classic ECG finding of sinus tachy-
cardia is the presence of sinus P wave in front of every
QRS complex with a PR interval of 0.12 seconds. The
morphology of the P wave in the 12-lead ECG differen-
tiates a sinus P wave from a P wave that is not of sinus
origin.
Frontal plane: Because the sinus node is located at
the upper right border of the right atrium close to
the entrance of the superior vena cava, the sinus im-
pulse spreads from right atrium to left atrium and
from top to bottom in the direction of 0 to 90, re-
sulting in upright P waves in leads I, II, and aVF
(Fig. 14.1). The axis of the sinus P wave is approxi-
mately 45 to 60; thus, the P wave is expected to be
upright in lead II. The hallmark of normal sinus
rhythm therefore is a positive P wave in lead II. If the
P wave is not upright in lead II, the P wave is proba-
bly ectopic (not of sinus node origin).
Horizontal plane: In the horizontal plane, the sinus
node is located at the posterior and right border of
the right atrium. Thus, the impulse travels anteriorly
Figure 14.1: Sinus Tachycardia. Because Sinus
Node
the sinus node is located at the upper border
of the right atrium, activation of the atria is
from right to left and from top to bottom
(arrows) resulting in upright P waves in leads I,
II, and aVF. RA, right atrium; LA, left atrium.
90
Lead aVF
180
and leftward causing the P waves to be upright in V3
to V6 (Fig. 14.2). This was previously discussed in
Chapter 7, Chamber Enlargement and Hypertrophy.
Pathologic Sinus Tachycardia
Sinus tachycardia: Sinus tachycardia accelerates and
decelerates gradually and is a classic example of a
tachycardia that is nonparoxysmal. Sinus tachycardia
usually has an identifiable cause, which could be phys-
iologic, such as exercise, emotion, fear, or anxiety. The
underlying condition may be pathologic, such as acute
pulmonary embolism, acute pulmonary edema, thyro-
toxicosis, infection, anemia, hypotension, shock, or
hemorrhage. It may be due to the effect of pharmaco-
logic agents such as atropine, hydralazine, epinephrine,
norepinephrine and other catecholamines.
Pathologic sinus tachycardia: Although sinus tachy-
cardia is appropriate and physiologic, it should be dif-
ferentiated from other types of sinus tachycardia that
are not associated with any identifiable cause. These
other types of tachycardia are primary compared with
normal sinus tachycardia, which is secondary to an un-
derlying condition or abnormality. Sinus tachycardia
without an identifiable cause is abnormal and can oc-
cur in the following conditions.
Inappropriate sinus tachycardia: This type of
sinus tachycardia is not associated with any underlying
condition and no definite causes can be identified.
0 Lead I
LA
RA The sinus P wave is upright in
leads I, II and aVF
AV Node
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Figure 14.2: Sinus Tachycardia. Twelve-lead electrocardiogram showing sinus tachycardia. Sinus tachycardia
is identified by the presence of upright P waves in leads I, II, and aVF and also in V3 to V6. The axis of the P wave is
closest to lead II, which is the most important lead in identifying the presence of sinus rhythm.
Very often, the rate of the tachycardia is inappropri-
ately high at rest or during physical activity. Increase
in sinus rate during exercise is very often out of pro-
portion to the expected level of response. The sinus
tachycardia is due to enhanced automaticity of the
cells within the sinus node.
Postural orthostatic tachycardia syndrome
(POTS): This is similar to inappropriate sinus tachy-
cardia except that the tachycardia is initiated by the
upright posture and is relieved by recumbency. In
POTS, there should be no significant orthostatic hy-
potension or autonomic dysfunction because sinus
tachycardia becomes appropriate when these enti-
ties are present.
Sinoatrial reentry: This tachycardia is a type of SVT
resulting from re-entry where the sinus node is part of
the reentrant pathway. When this occurs, the P waves
resemble that of sinus tachycardia. It is paroxysmal in
contrast to the other types of sinus tachycardia that
are nonparoxysmal. This tachycardia will be discussed
in more detail under SVT from sinoatrial reentry.
Sinus Tachycardia
The 12-lead ECG alone cannot differentiate physiologic
sinus tachycardia from sinus tachycardia that is patho-
logic and inappropriate because the ECG findings of
Sinus Tachycardia 181
these two clinical entities are identical. The diagnosis of
pathologic sinus tachycardia therefore is based on addi-
tional clinical information demonstrating that the sinus
tachycardia is not associated with any underlying con-
dition. Continuous monitoring is often helpful in
demonstrating that the tachycardia is inappropriate. It
is also helpful in showing that the sinus tachycardia can
be paroxysmal and can be precipitated or terminated by
premature atrial complexes, suggesting that the tachy-
cardia is due to sinoatrial reentry.
The following ECG shows sinus tachycardia (Fig. 14.2).
The P waves are upright in leads I, II, and aVF and in V3
to V6. Each P wave is in front of the QRS complex with
a PR interval of 0.12 seconds.
Summary of ECG Findings
1. Sinus P waves are present with a rate >100 bpm.
2. The sinus P waves precede each QRS complex with a PR in-
terval 0.12 seconds.
3. The morphology of the P wave should be upright in leads I,
II, and aVF and in V3 to V6.
Mechanism
The sinus impulse arises from the sinus node, which contains
automatic cells with pacemaking properties. Pacemaking cells
exhibit slow spontaneous diastolic depolarization during
phase 4 of the action potential (see Chapter 1, Basic Anatomy
LWBK271-C14_180-183.qxd 29/1/09 9:06 pm Page 182 LWBK270-4119G-C02_073-110.qxd
182 Chapter 14
and Electrophysiology). The sinus node has the fastest rate of
spontaneous depolarization occurring more than one per
second. As a result, the rhythm originating from the sinus
node is the most dominant and is the pacemaker of the heart.
The rate of the sinus node is usually modified by a number of
stimuli, most notably sympathetic and parasympathetic
events, but it could also be influenced by other conditions
such as stretch, temperature, and hypoxia. It responds appro-
priately to physiologic as well as pathologic stimuli. When
the sinus tachycardia is inappropriate, it may be due to en-
hance firing rate of the automatic cells in the sinus node or
autonomic regulation of the sinus node may be abnormal
with increased response to sympathetic stimuli or decreased
response to parasympathetic influences.
Pacemaker cells are not localized to a specific area, but are
widely distributed throughout the sinus node. Cells with
faster rates occupy the more cranial portion, whereas cells
with slower rates occupy the more caudal portion of the
sinus node. During sinus tachycardia, the impulses do not
originate from a single stationary focus, but migrate from a
caudal area to a more cranial location as the rate of the tachy-
cardia increases. This shift in the origin of the sinus impulse
to a more cranial location may change the morphology of the
P wave, resulting in a P wave axis that is slightly more vertical
(toward 90) during faster heart rates and slightly more hor-
izontal (toward 0) during slower sinus rates. This change in
the origin of the impulse during sinus tachycardia has clini-
cal and therapeutic implications. Patients with inappropriate
sinus tachycardia, where the primary abnormality is due to
inappropriate increase in automaticity in the sinus node cells
and are refractory to medical therapy, may respond to selec-
tive ablation of certain portions of the sinus node.
Clinical Implications
Sinus tachycardia is a physiologic mechanism occurring ap-
propriately in response to known stimuli. This includes
hypotension, fever, anemia, thyrotoxicosis, and pain, among
other things.
Sinus tachycardia is appropriate when it is due to a secondary
cause. Sinus tachycardia however may be difficult to differen-
tiate from SVT, especially if the P waves are obscured by the
T waves of the preceding complex. The clinical significance
Treatment
and therapy of sinus tachycardia are different from that of
SVT, and every attempt should be made to differentiate one
from the other.
Although sinus tachycardia is usually physiologic and appro-
priate in response to a variety of clinical conditions, sinus
tachycardia may result in unnecessary increase in heart rate
without a definite secondary cause. When this occurs, the
sinus tachycardia is abnormal and could be due to inappro-
priate sinus tachycardia, postural orthostatic tachycardia
syndrome, or sinoatrial reentrant tachycardia.
Inappropriate sinus tachycardia: Sinus tachycardia is
inappropriate when there is no known cause for the sinus
tachycardia. Inappropriate sinus tachycardia occurs usu-
ally in young females in their 30s. Most are health care
workers. Inappropriate sinus tachycardia is important to
differentiate from appropriate sinus tachycardia because
the abnormality may reside in the sinus node itself due to
inappropriate enhancement in automaticity of the sinus
node cells rather than due to secondary causes.
POTS: This type of sinus tachycardia is similar to inap-
propriate sinus tachycardia except that the tachycardia is
triggered by the upright posture and is relieved by recum-
bency. The tilt table test may result in increase in heart
rate 30 bpm from baseline or increase in heart rate
120 bpm without significant drop in blood pressure.
The drop in blood pressure should not be 30 mm Hg
systolic or 20 mm Hg mean blood pressure within
3 minutes of standing or tilt. The cause of POTS is multi-
factorial and approximately half of patients have an-
tecedent viral infection. It may be due to the presence of a
limited autonomic neuropathy associated with postgan-
glionic sympathetic denervation of the legs, resulting in
abnormality in vasomotor tone and blood pooling. It may
also be due to a primary abnormality of the sinus node
cells similar to inappropriate sinus tachycardia. Other sec-
ondary causes such as venous pooling in the splanchnic
bed, hypovolemia, or failure to vasoconstrict have also
been implicated. Because the abnormality in POTS may
be in the sinus node itself (primary), but could also be
due to abnormalities outside the sinus node (secondary
causes), response to therapy may be difficult to predict.
Thus, therapy to suppress sinus node automaticity with
the use of pharmacologic agents or radiofrequency mod-
ification of the sinus node may be appropriate if the ab-
normality is in the sinus node itself, but may not be effec-
tive if the abnormality is due to secondary causes.
Sinoatrial reentrant tachycardia: This is further dis-
cussed in Chapter 17, Supraventricular Tachycardia due to
Reentry. The tachycardia can be precipitated or terminated
by a premature ectopic atrial impulse. Unlike the other
types of sinus tachycardia, sinoatrial reentrant tachycardia
is usually associated with structural cardiac disease.
Sinus tachycardia: Appropriate sinus tachycardia does not
need any pharmacologic therapy to suppress the arrhythmia.
The underlying cause of the tachycardia should be recog-
nized and corrected.
Occasionally, sinus tachycardia may occur in a setting that
is not advantageous to the patient. For example, sinus
tachycardia may be related to pericarditis, acute myocar-
dial infarction, congestive heart failure, or thyrotoxicosis.
In these patients, it may be appropriate to slow down the
heart rate with beta blockers and identify other causes of
sinus tachycardia that can be corrected. Beta blockers are
standard drugs for congestive heart failure resulting from
LWBK271-C14_180-183.qxd 29/1/09 9:06 pm Page 183 LWBK270-4119G-C02_073-110.qxd
systolic dysfunction as well as for patients with acute my-
ocardial infarction, whether or not sinus tachycardia is
present. It is also commonly used to control sinus tachy-
cardia associated with thyrotoxicosis.
Inappropriate sinus tachycardia: If secondary causes have
been excluded and the sinus tachycardia is deemed inappro-
priate, therapy includes beta blockers and nondihydropyri-
dine calcium channel blockers such as diltiazem and vera-
pamil. Beta blockers may be used as first-line therapy unless
these agents are contraindicated. In patients who are resist-
ant to pharmacologic therapy or patients who are unable to
take oral therapy, sinus node modification using radiofre-
quency ablation has been used successfully. This carries a risk
of causing sinus node dysfunction and permanent pacing
and should be considered only as a last resort.
POTS: Because the cause of POTS may be a primary sinus
node abnormality but could also be due to secondary causes,
response to therapy is unpredictable.
Nonpharmacologic therapy: Volume expansion may
be required with proper regular oral hydration combined
with high-sodium intake of up to 10 to 15 g daily, use of
compressive stockings, sleeping with the head of the bed
tilted up, and resistance training such as weight lifting.
Pharmacologic therapy: Pharmacologic therapy has
been shown to provide short-term, partial relief of symp-
toms in approximately half of patients, regardless of the
agent used.
n Beta blockers: If nonpharmacologic therapy is not
effective, low-dose beta blockers such as propranolol
20 to 30 mg three to four times daily may be tried be-
cause the abnormality may be in the sinus node cells
or the result of hypersensitivity to endogenous beta
agonists.
n Calcium channel blockers: If beta blockers are not
effective or are contraindicated because of bron-
chospastic pulmonary disease, calcium channel block-
ers such as diltiazem or verapamil may be given. These
drugs are contraindicated when there is left ventricu-
lar systolic dysfunction.
n Mineralocorticoids: Mineralocorticoids, such as flu-
drocortisone 0.1 to 0.3 mg orally once daily, may be
useful when there is hypovolemia, which is often seen
in POTS. This should be considered only after non-
pharmacologic therapy has been tried. These agents
are usually combined with hydration and high sodium
intake.
n Adrenoceptor agonists: Adrenoceptor agonist such as
midodrine 2.5 to 10 mg three times daily orally has
been shown to improve symptoms during tilt table
testing, although its efficacy during long-term therapy
is not known.
Sinus Tachycardia 183
n Serotonin reuptake inhibitors: Response to selective
serotonin reuptake inhibitors is similar to that of
other pharmacologic agents.
Catheter ablation: Although catheter ablation or catheter
modification has been performed in some patients with
POTS, response to this type of therapy may be difficult to
predict because the abnormality may be primarily in the
sinus node but could also be due to secondary causes.
Prognosis
Appropriate sinus tachycardia: Sinus tachycardia is phys-
iologic and is an expected normal response to a variety of
clinical situations. The overall prognosis of a patient with si-
nus tachycardia depends on the underlying cause of the sinus
tachycardia and not the sinus tachycardia itself.
Pathologic sinus tachycardia: Therapy for pathologic si-
nus tachycardia is given primarily to improve the quality of
life rather than to prolong survival. In supraventricular
tachycardia from sinoatrial reentry, the tachycardia may be
associated with structural cardiac disease. The prognosis will
depend on the nature of the underlying cause. Pathologic
sinus tachycardia has not been shown to cause tachycardia
mediated cardiomyopathy.
POTS: Up to 80% of patients with POTS improve with most
returning to normal functional capacity. Those with an-
tecedent viral infection seem to have a better outcome.
Suggested Readings
Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
ACC/AHA/ESC guidelines for the management of patients
with supraventricular arrhythmiasexecutive summary: a
report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines, and the
European Society of Cardiology Committee for Practice
Guidelines (Writing Committee to Develop Guidelines for
the Management of Patients With Supraventricular Arrhyth-
mias). J Am Coll Cardiol. 2003;42:1493531.
Freeman R, Kaufman H. Postural tachycardia syndrome. 2007
UptoDate. www.utdol.com.
Sandroni P, Opfer-Gehrking TL, McPhee BR, et al. Postural
tachycardia syndrome: clinical features and follow-up study.
Mayo Clin Proc. 1999;74:11061110.
Singer W, Shen WK, Opfer-Gehrking TL, et al. Evidence of an
intrinsic sinus node abnormality in patients with postural
tachycardia syndrome. Mayo Clin Proc. 2002;77:246252.
Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic
tachycardia syndrome: the Mayo Clinic experience. Mayo
Clin Proc. 2007;82:308313.
Yussuf S, Camm J. Deciphering the sinus tachycardias. Clin Car-
diol. 2005;28:267276.
LWBK271-C15_184-186.qxd 29/1/09 7:43 pm Page 184 LWBK270-4119G-C02_073-110.qxd
15
Supraventricular Tachycardia
Introduction
Tachycardia refers to a heart rate 100 beats per minute
(bpm). The tachycardia may be supraventricular or
ventricular depending on the origin of the arrhythmia.
Supraventricular tachycardia (SVT): If the tachy-
cardia originates above the bifurcation of the bundle
of His, usually in the atria or atrioventricular (AV)
junction, the tachycardia is supraventricular (Fig.
15.1A). Supraventricular impulses follow the nor-
mal AV conduction system, activate the ventricles
synchronously and will have narrow QRS complexes
measuring 120 milliseconds. The QRS may be
wide if there is preexistent bundle branch block,
ventricular aberration, or the impulse is conducted
through a bypass tract.
A. Supraventricular B. Ventricular
Tachycardia Tachycardia
Atria Atria
Bifurcation of
the Bundle of
His
Ventricles Ventricles
Figure 15.1:Supraventricular and Ventricular
Tachycardia (VT). (A) In supraventricular tachycardia, the im-
pulses originate above the bifurcation of the bundle of His, fol-
low the normal AV conduction system, and activate both ventri-
cles synchronously resulting in narrow QRS complexes. (B) In VT,
the impulses originate below the bifurcation of the bundle of
His. Activation of the ventricles is not synchronous because the
impulse has to spread outside the normal conduction system
resulting in wide QRS complexes. The stars represent the origin
of the impulse. The horizontal line represents the bifurcation of
the bundle of His.
184
Ventricular tachycardia (VT): If the tachycardia
originates below the bifurcation of the bundle of
His, the tachycardia is ventricular (Fig. 15.1B). The
impulse will spread to the ventricles outside the nor-
mal AV conduction system. Activation of the ventri-
cles will not be synchronous resulting in wide QRS
complexes measuring 120 milliseconds.
There are other types of tachycardias with narrow QRS
complexes other than SVT. These include sinus tachy-
cardia, atrial flutter, and atrial fibrillation. These tachy-
cardias should be distinguished from each other be-
cause the treatment of these various arrhythmias is
different.
Sinus tachycardia: Sinus tachycardia implies that
the rhythm originates from the sinus node with a
rate that exceeds 100 bpm. Sinus tachycardia is a
normal finding, which is usually an appropriate
response to a physiologic or pathologic condition.
This was previously discussed in Chapter 14, Sinus
Tachycardia.
Atrial flutter: The diagnosis of atrial flutter is based
on the presence of a very regular atrial rate of 300 
50 bpm. This will be discussed separately in Chap-
ter 18.
Atrial fibrillation: The diagnosis of atrial fibrilla-
tion is based on an atrial rate of 400  50 bpm with
characteristic baseline fibrillatory pattern and irreg-
ularly irregular R-R intervals. This will also be dis-
cussed separately.
Table 15.1 classifies the different types of narrow com-
plex tachycardias.
SVT: SVT is a narrow complex tachycardia originating
outside the sinus node but above the bifurcation of the
bundle of His, with a rate that exceeds 100 bpm. Several
types of SVT are present and are classified according to
three general mechanisms: reentry, enhanced auto-
maticity, and triggered activity.
Reentry: SVT due to reentry is an abnormality in
the propagation of the electrical impulse resulting
from the presence of two separate pathways with
different electrophysiologic properties (Fig. 15.2A).
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Supraventricular Tachycardia 185

TABLE 15.1

Narrow Complex Tachycardia

Sinus Atrial Atrial
Tachycardia SVT Flutter Fibrillation
Sinus Rate Reentrant Automatic Atrial Rate Atrial Rate
100 AVNRT Atrial 300  50 400  50
AVRT  Focal or unifocal

Intraatrial  Multifocal

Sinoatrial Junctional
 Paroxysmal

 Nonparoxysmal

Atrial Rate 200  50

Table shows the different tachycardias that can result in narrow QRS complexes. Generally, the atrial
rate of atrial fibrillation is 400  50 bpm, for atrial flutter 300  50 bpm, for SVT approximately
200  50 and for sinus tachycardia 100 bpm. AVNRT, atrioventricular nodal reentrant tachycardia;
AVRT, atrioventricular reciprocating tachycardia; SVT, supraventricular tachycardia.

Enhanced automaticity: This is an abnormality in
initiation rather than conduction of the electrical
impulse. Some cells in the atria or AV junction may
exhibit phase 4 diastolic depolarization and may
spontaneously discharge faster than that of the sinus
node if the discharge rate is enhanced (Fig. 15.2B).
Triggered activity: This is also an abnormality
in initiation of the electrical impulse resulting from
occurrence of afterdepolarizations. Afterdepolariza-
tions are secondary depolarizations that are triggered
by the initial impulse (Fig. 15.2C). The afterdepolar-
ization does not always reach threshold potential, but
when it does, it may be followed by repetitive firing of
the membrane voltage. Triggered activity is usually
seen in association with digitalis toxicity, calcium ex-
cess, or increased catecholamines.
SVT from reentry usually occurs in normal individuals
without evidence of structural cardiac disease. SVT from
enhanced automaticity may occur in normal individu-
als, although they are more frequently associated with
structural cardiac diseases, abnormalities in electrolytes
and blood gasses, or use of pharmacologic agents. SVT
from triggered activity usually occurs with digitalis ex-
cess or after cardiac surgery. The differences between
SVT from reentry, from enhanced automaticity, and
from triggered activity are summarized in Table 15.2.

Initial Early Late

Slow Pathway Slow diastolic depolarization Impulse Afterdepolarizations Afterdepolarizations
1
1
2 2

0 0 0 0 3
3

Fast Pathway 4 4
4 4 4
A B C

Figure 15.2: Mechanisms of Supraventricular tachycardia (SVT). (A) Reentry is the most common mecha-
nism of all SVT. In reentry, two separate pathways with different electrophysiologic properties are present.
(B) Diagram of action potential of a cell with automatic properties.These cells exhibit slow phase 4 diastolic depo-
larization, which may dominate as the pacemaker if the discharge rate is enhanced. (C) Diagram of action potential
of a cell with triggered activity. Oscillations occur early during phase 2 or phase 3, or late during phase 4 of the
action potential. The dotted horizontal lines in (B) and (C) represent threshold potential. Numbers 0 to 4 represent
the different phases of the action potential. Adapted and modified from Wellens and Conover.
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186 Chapter 15

TABLE 15.2

Differences between SVT because of Reentry, Enhanced Automaticity, and Triggered Activity
Reentry Enhanced Automaticity Triggered Activity
Mechanism This is an abnormality in This is an abnormality in impulse Early or late after-
impulse conduction. A initiation. Cells with automatic depolarizations are present.
reentrant circuit is present. properties become the
dominant pacemaker.
Initiation Initiated by premature Initiated by increased firing rate Initiation is not well defined.
impulses or by rapid pacing. of automatic cells in the atria or
AV junction.
Termination Terminated by vagal maneuvers, Not usually terminated by vagal May be terminated by
\ AV nodal blockers, ectopic maneuvers, AV nodal blockers, premature impulses,
impulses, overdrive pacing, or ectopic impulses, overdrive overdrive pacing, or
electrical cardioversion. pacing or electrical cardioversion. electrical cardioversion.
Underlying Frequently seen in structurally Frequently seen in patients with Frequently seen in patients
Condition normal hearts. metabolic or pulmonary with digitalis toxicity or
disorders or patients on postcardiac surgery.
adrenergic drugs, caffeine,
theophylline, or other agents.
Examples of AV nodal reentry AT Atrial tachycardia with 2:1
SVT AV reentry  Focal AT AV block
Sinoatrial reentry  Multifocal AT Nonparoxysmal junctional
Intraatrial reentry Junctional tachycardia tachycardia
 Focal or paroxysmal

 Nonparoxysmal

SVT, supraventricular tachycardia; AT, atrial tachycardia; AV, atrioventricular.

Wit AL, Rosen MR. Cellular electrophysiology of cardiac ar-

Suggested Readings rhythmias. Part I. Arrhythmias caused by abnormal im-
pulse generation. Mod Concepts Cardiovasc Dis. 1981;
50:16.
Conover MB. Arrhythmogenesis. In: Understanding Electrocar-
Wit AL, Rosen MR. Cellular electrophysiology of cardiac ar-
diography. 5th ed. St. Louis: Mosby; 1988:3141.
rhythmias. Part II. Arrhythmias caused by abnormal im-
Wellens HJJ, Conover M. Drug induced arrhythmic emergencies.
In: The ECG in Emergency Decision Making. 2nd ed. St. Louis: pulse conduction. Mod Concepts Cardiovasc Dis. 1981;
50:712.
Saunders Elsevier; 2006:178.
LWBK271-C16_187-210.qxd 1/30/09 11:24 AM Page 187 Aptara Inc.

Supraventricular Tachycardia
due to Reentry
Types of Reentrant Supraventricular
Tachycardia
Supraventricular tachycardia (SVT) from reentry:
This accounts for approximately 80% to 90% of all sus-
tained SVT in the general population. Reentrant SVT
results from abnormal propagation of the electrical
impulse because of the presence of two separate path-
ways with different electrophysiologic properties.
There are four types of SVT from reentry. They are di-
agrammatically shown in Figure 16.1AD.
Atrioventricular nodal reentrant tachycardia
(AVNRT): The reentrant circuit consists of a slow
and fast pathway that circles around the AV node
(Fig. 16.1A).
Atrioventricular reciprocating (or reentrant)
tachycardia (AVRT): The tachycardia is associated
16
with a bypass tract connecting the atrium directly to
the ventricle (Fig. 16.1B).
Sinoatrial reentrant tachycardia (SART): The
tachycardia involves the sinus node and contiguous
atrium (Fig. 16.1C).
Intra-atrial reentrant tachycardia (IART): The
tachycardia is confined to a small circuit within the
atrium (Fig. 16.1D).
Atrioventricular Nodal
Reentrant Tachycardia
AVNRT: AVNRT is the most common SVT occurring in
the general population. It usually affects young and healthy
individuals without evidence of structural heart disease
and is twice more common in women than in men.

Sinus node

Bypass
tract

A B C D

Figure 16.1: Supraventricular Tachycardia (SVT) from Reentry. (A) AV nodal reentrant
tachycardia. The two pathways circle the AV node. This is the most common, occurring in more than
60% of all reentrant narrow complex tachycardia. (B) AV reciprocating tachycardia. This type of SVT is as-
sociated with a bypass tract connecting the atrium and ventricle. This is the next common occurring in
approximately 30% of all reentrant SVT. (C) Sinoatrial reentrant tachycardia. The reentrant circuit involves
the sinus node and adjacent atrium. This type of SVT is rare. (D) Intraatrial reentrant tachycardia. A micro-
reentrant circuit is present within the atria. This type of SVT is also rare. The red circles represent the
reentrant circuit.The arrows point to the direction of the reentrant circuit. AV, atrioventricular.

187
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188 Chapter 16

Figure 16.2: Diagrammatic Representation of P waves are inverted

the Electrical Circuit in Atrioventricular Nodal in leads II, III and aVF
Reentrant Tachycardia (AVNRT). Two separate Exit to Atria
pathways are present around the AV node, the slow path-
way (dotted line), which conducts the impulse slowly and
has a shorter refractory period and the fast pathway (solid Fast Pathway
Slow Pathway
line), which conducts rapidly and has a longer refractory Conducts slowly AV Conducts rapidly
period. The impulse circles the AV node repeatedly using Shorter refractory Node Longer refractory
period period
these two separate pathways causing a reentrant tachy-
cardia called AVNRT.

Exit to Ventricles

QRS complexes are

narrow

AVNRT is a type of reentrant SVT with two separate

pathways. These two pathways have different electro-
physiologic properties and are both located within or
around the AV node.
Slow pathway: The slow pathway has a shorter re-
fractory period.
Fast pathway: The fast pathway has a longer re-
fractory period.
The slow pathway conducts the impulse anterogradely
from atrium to ventricles. The QRS complex is narrow
because the impulse follows the normal AV conduction
system. The fast pathway conducts the impulse retro-
gradely to the atria. Because the atria are activated from
below upward in a caudocranial direction, the P waves
are inverted in leads II, III, and aVF (Fig. 16.2).
AVNRT
Mechanism of AVNRT: AVNRT is triggered by a pre-
mature impulse originating from the atria or ventricles.
The premature atrial impulse should be perfectly
timed to occur when the slow pathway has fully re-
covered from the previous impulse and the fast
pathway is still refractory because of its longer re-
fractory period. The premature atrial impulse enters
the slow pathway, but is blocked at the fast pathway
(Fig. 16.3, #1 and #2).
When the impulse reaches the end of the slow
pathway, it can exit through the bundle of His to
activate the ventricles (#3) and at the same time

Figure 16.3:Mechanism of AV Nodal Sinus Rhythm AVNRT

Reentrant Tachycardia. A premature
atrial complex (PAC) is conducted
anterogradely through the slow pathway
but is blocked at the fast pathway.The
#1. Premature
impulse activates the ventricles and at the atrial impulse PAC
same time is conducted retrogradely enters the slow Atria
through the fast pathway to activate the pathway but is
blocked at the #5. Impulse activates the
atria resulting in reentry (see text). AVNRT, fast pathway atria retrogradely and
atrioventricular nodal reentrant tachycardia. reenters the slow pathway
Slow
Pathway
Fast
#2. The impulse is AV Pathway
conducted Node
anterogradely #4. Impulse is conducted
through the slow retrogradely through the
pathway fast pathway

#3. The ventricles

are activated
synchronously Ventricles
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Supraventricular Tachycardia due to Reentry 189

A Figure 16.4: Diagrammatic Representation

V
of Atrioventricular Nodal Reentrant
Atria
N NO P Waves
Tachycardia (AVNRT). AVNRT is classically
R
T recognized as a narrow complex tachycardia with
regular R-R intervals and no P waves. A complete
12-lead electrocardiogram of AVNRT is shown in
Figure 16.5.
Ventricles

circles back through the fast pathway, which by now
is fully recovered, to activate the atria retrogradely
(#4 and #5).
The impulse can reenter the slow pathway and trav-
els the same circuit repetitively causing a reentrant
tachycardia called AVNRT.
Electrocardiogram (ECG) findings: The most com-
mon ECG presentation of AVNRT is the presence of a
narrow complex tachycardia with regular R-R intervals
and no visible P waves (Figs. 16.4 and 16.5). The P
waves are retrograde and are inverted in leads II, III,
and aVF, but are not visible in the ECG because the
atria and ventricles are activated simultaneously;
hence, the P waves are buried within the QRS com-
plexes. This is the most common presentation occur-
ring in 66% of all cases of AVNRT.
Other ECG patterns of AVNRT: In AVNRT, activation
of the atria and ventricles may not be perfectly syn-
chronous. If the retrograde P wave occurs immediately
after the QRS complex, it may be mistaken for S wave
in leads II, III, and aVF or r in V1. If the retrograde P
wave occurs immediately before the QRS complex, it
may be mistaken for q wave in lead II, III, or aVF (Fig.
16.6). These pseudo-Q, pseudo-S, and pseudo-r waves
should resolve on conversion of the tachycardia to nor-
mal sinus rhythm (Fig. 16.7).
Examples of pseudo-S waves in leads II or pseudo-r in
V1 are shown (See Figs 16.8 to 16.10). This pattern is
diagnostic of AVNRT and is seen in approximately 30%
of all cases. The pseudo-S waves in lead II and pseudo-
r in V1 are retrograde P waves, but are commonly mis-
taken as part of the QRS complex. These P waves
should resolve when the AVNRT converts to normal si-
nus rhythm, as shown in Figures 16.7 and 16.8.
AVNRT can also manifest in the ECG by the presence
of retrograde P waves much further away from the QRS

Figure 16.5: Twelve-Lead Electrocardiogram of Atrioventricular Nodal Reentrant Tachycardia

(AVNRT). No P waves.Twelve-lead electrocardiogram showing AVNRT. The retrograde P waves are superimposed
within the QRS complexes and are not visible in any of the 12 leads. This is the most common presentation of AVNRT.
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190 Chapter 16

Retrograde Retrograde
II P waves P waves

Atria

Pseudo-s waves Pseudo-Q waves

Retrograde
P waves Pseudo-r waves
V1
Ventricles

Figure 16.6:Pseudo-S and Pseudo-R' waves in Atrioventricular Nodal Reen-

trant Tachycardia (AVNRT). In AVNRT, the retrograde P waves may emerge at the
beginning or terminal portion of the QRS complexes and can be mistaken for pseudo-Q or
pseudo-S waves in leads II, III, and aVF or as pseudo r waves in V1. These pseudo-q and
pseudo-s waves in lead II and pseudo-r in V1 should resolve upon conversion of the tachy-
cardia to normal sinus rhythm (see Fig. 16.7).

complexes. The retrograde P waves may distort the ST
segment rather than the terminal portion of the QRS
complex as shown in Figures 16.11 and 16.12. Gener-
ally, when the P waves are no longer connected to the
QRS complexes, the SVT is more commonly the result
of AVRT rather than AVNRT.
Atypical AVNRT: Finally, AVNRT can also manifest
with retrograde P waves preceding each QRS complex
(Figs. 16.13 and 16.14). This type of AVNRT is called
atypical or uncommon and occurs infrequently. The
tachycardia is initiated by an ectopic ventricular (rather
than atrial) impulse. The impulse is retrogradely con-
ducted to the atria through the slow pathway and an-
terogradely conducted to the ventricles through the fast
pathway. This type of SVT may be difficult to differenti-
ate from other narrow complex tachycardias, especially
focal atrial tachycardia.
AVNRT therefore has many possible ECG presenta-
tions and should be considered in any narrow complex
tachycardia with regular R-R intervals whether or not
retrograde P waves can be identified.
Summary of ECG findings: Figure 16.15 is a sum-
mary of the different ECG patterns of AVNRT as
recorded in lead II.
Typical AVNRT: Figures 16.15AD are examples of
typical AVNRT. The impulse is conducted antero-
gradely to the ventricles through the slow pathway
and retrogradely to the atria through the fast path-
way (slow/fast circuit).
Atypical AVNRT: Figure 16.15E is an example of
atypical AVNRT. The impulse is conducted antero-
gradely to the ventricles through the fast pathway
and retrogradely to the atria through the slow path-
way (fast/slow circuit).

Lead II

Lead V1

AVNRT Normal Sinus Rhythm

Figure 16.7: Atrioventricular Nodal Reentrant Tachycardia (AVNRT) Before and After Con-
version to Sinus Rhythm. Note the presence of pseudo-S waves in lead II and pseudo r waves in V1
(left panel, circled) during AVNRT, which resolve on conversion to normal sinus rhythm.
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Supraventricular Tachycardia due to Reentry 191

A. During tachycardia Pseudo-r waves

Figure 16.8:Atrioventricular
Nodal Reentrant Tachycardia
(AVNRT) with Pseudo-S and
Pseudo-R' waves. Complete 12-
lead electrocardiogram during
AVNRT is shown (A). Note the
pseudo-S waves in leads II and aVF
and pseudo-r in V1 (arrows), which
are no longer present on conversion
of the AVNRT to normal sinus
rhythm (B).

B. Upon conversion to normal sinus rhythm

A. During Tachycardia Figure 16.9:Spontaneous

Conversion of Atrioventricu-
lar Nodal Reentrant Tachycar-
dia (AVNRT) to Normal Sinus
Rhythm. (A) A 12-lead ECG
during AVNRT showing pseudo-S
waves in lead II (arrows). (B) Lead II
rhythm strip recorded from the
same patient during tachycardia
(left half of rhythm strip) and after
spontaneous conversion to normal
sinus rhythm (right half of rhythm
strip). Note that the pseudo-S
waves during AVNRT have
disappeared (arrow).

Pseudo-S waves have disappeared upon

B. Pseudo-S waves conversion to sinus rhythm
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Lead II

Figure 16.10: Conversion of Atrioventricular Nodal Reentrant Tachycardia

(AVNRT) to Normal Sinus Rhythm with Adenosine. Adenosine is the drug of choice
in converting AVNRT to normal sinus rhythm. The initial portion of the rhythm strip shows a
narrow complex tachycardia with pseudo-S waves (arrows) in lead II consistent with AVNRT.
Note the disappearance of the pseudo-S waves on conversion to sinus rhythm. Note also that
the tachycardia terminated with a pseudo-S wave (last arrow), implying that the reentrant cir-
cuit was blocked at the slow pathway.

AVNRT: Retrograde P waves occurring after the QRS complexes

Figure 16.11: Other Patterns of Atrioventricular Nodal Reentrant

Tachycardia (AVNRT). Retrograde P waves (arrows) occur immediately af-
ter the QRS complexes and distort the ST segment or T waves of the previous
complex. Although this pattern is consistent with AVNRT, this is more
commonly the result of atrioventricular reentrant tachycardia.

A.

B.

Figure 16.12: Twelve-lead Electrocardiogram Showing Other Presentations of Atrioventricular

Nodal Reentrant Tachycardia (AVNRT). Twelve-lead electrocardiogram (A) and lead II rhythm strip from the
same patient (B) showing retrograde P waves that are further away from the QRS complexes (arrows). Although this
pattern is more typically seen in atrioventricular reentrant tachycardia, electrophysiologic study in this patient con-
firmed the presence of AVNRT with successful ablation of the slow pathway.

192
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Supraventricular Tachycardia due to Reentry 193

SP FP

Atypical AVNRT: Retrograde P waves in front of the QRS complexes

Figure 16.13: Diagrammatic Representation of Atypical Atrioventricular

Nodal Reentrant Tachycardia (AVNRT). Retrograde P waves (arrows) occur before the
next QRS complex with R-P interval longer than PR interval. The impulse is conducted retro-
gradely through the slow pathway (SP) and anterogradely through the fast pathway (FP).

ECG Findings of AVNRT
1. AVNRT is typically a narrow complex tachycardia with regular
R-R intervals and no P waves.
2. When P waves are present, they are always retrograde because
the atria are activated from below upward. The P waves there-
fore are inverted in leads II, III, and aVF.
3. Retrograde P waves may be present but may not be recognized
when they are embedded within the QRS complexes. When
the retrograde P waves distort the terminal portion of the QRS
complexes, they can be mistaken for S waves in II, III, and aVF
or r in V1. In rare instances, the retrograde P waves may dis-
tort the initial portion of the QRS complex and mistaken for q
waves in lead II, III, and aVF.
4. The retrograde P waves may be inscribed immediately after
the QRS complexes deforming the ST segment or T wave of
the previous complex.
5. The retrograde P waves may be inscribed before the QRS
complex. This type of AVNRT is called atypical or uncom-
mon. Other atypical forms may be associated with retro-
grade P waves midway or almost midway between the QRS
complexes.
6. The presence of second-degree AV block during tachycardia is
possible but is rare and makes the diagnosis of AVNRT highly
unlikely.
7. The ventricular rate in AVNRT varies from 110 to 250 beats
per minute (bpm). The rate, however, is not helpful in distin-
guishing AVNRT from other types of SVT.

Figure 16.14: Twelve-lead Electrocardiogram of Atypical Atrioventricular Nodal Reentrant Tachy-

cardia (AVNRT). Inverted P waves are seen before the QRS complexes in leads II, III and aVF (arrows). Although
this pattern is more commonly seen in other types of supraventricular tachycardia such as focal atrial or junctional
tachycardia, this type of electrocardiogram can also occur in patients with atypical AVNRT.
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194 Chapter 16

Figure 16.15: Summary of the Differ- ECG of AVNRT in Lead II

ent Patterns of Atrioventricular
Nodal Reentrant Tachycardia
(AVNRT). (AE) The different possible
electrocardiogram patterns of AVNRT in lead
II. Arrows identify the retrograde P waves.
No P waves. This is the most common
A presentation of AVNRT occurring in
66% of all cases. The P waves are
centered within the QRS complexes.

B Pseudo S waves: 30%

C Pseudo q waves: 4%.

Retrograde P waves after the QRS

D complex. This is rare and is almost
always due to AVRT.

Atypical AVNRT: This is rare and is

E more commonly due to focal atrial
tachycardia.

8. AVNRT should always be considered as a possible diagnosis in
any narrow complex tachycardia with regular R-R intervals,
regardless of the presence or absence of retrograde P waves be-
cause this is the most common type of SVT.
Mechanism
AVNRT is an example of microreentry associated with a cir-
cuit within or around the AV node. The reentrant circuit
consists of two separate pathways with different electrical
properties. The slow pathway has a short refractory period
and the fast pathway has a longer refractory period. The
tachycardia is precipitated by an ectopic impulse originating
from the atria or ventricles. The impulse has to occur when
one pathway is still refractory and the other has completely
recovered. The tachycardia has a narrow QRS complex be-
cause the impulse follows the normal conduction system and
activates the ventricles normally. The rate of the tachycardia
is very regular because the impulse follows a fixed circuit.
Second-degree AV block is unusual but is possible during
AVNRT. It can potentially occur at the level of the His bundle
or more distally, which is extremely rare when the tachycar-
dia has narrow QRS complexes.
There are two types of AVNRT: typical and atypical.
Typical presentation: This is the most common presen-
tation of AVNRT occurring in more than 90% of all cases.
The slow pathway conducts the impulse to the ventricles
and the fast pathway conducts the impulse to the atria.
This type of AVNRT is often called the slow/fast circuit.
n No P Waves: This is the most typical and most common
presentation, occurring in approximately 66% of all
AVNRT. The atrial impulse is conducted anterogradely
to the ventricles through the slow pathway and retro-
gradely to the atria through the fast pathway. Activation
of both atria and ventricles are simultaneous; thus, the
P waves and QRS complexes are inscribed synchro-
nously and no P waves are evident in the ECG.
n Retrograde P waves: When P waves are present, they
are inverted in leads II, III, and aVF because the atria
are activated from below upward. The P waves may
deform the terminal portion of the QRS complexes
and mistaken for S waves in II, III, and aVF or r in V1.
This occurs in approximately 30% of all AVNRT. The
retrograde P waves may deform the initial portion of
the QRS complex and mistaken for q waves in II, III,
and aVF. This occurs in 4% of all AVNRT. The retro-
grade P waves may also deform the ST segment or the
initial portion of the T wave, although this type of
AVNRT is rare.
Atypical presentation: The fast pathway conducts the
impulse to the ventricles and the slow pathway conducts
the impulse to the atria. This fast/slow circuit is rare.
n The atypical form is characterized by retrograde P
waves in front of the QRS complexes. This is often
precipitated by an ectopic ventricular impulse retro-
gradely conducted to the atria through the slow path-
way and anterogradely conducted to the ventricles
through the fast pathway.
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n Other atypical forms may be associated with retro-
grade P waves midway or almost midway between the
QRS complexes.
Clinical Significance
SVT from reentry is the most common sustained narrow
complex tachycardia in the general population accounting
for approximately 80% to 90% of all SVT. Among the SVT
due to reentry, AVNRT is the most common occurring in
more than 60% of all reentrant SVT. AVNRT is frequently
seen in normal healthy individuals without structural car-
diac disease and is more common in females.
AVNRT can occur suddenly and terminate abruptly and is
therefore paroxysmal. This contrasts with sinus tachycardia
where the tachycardia is nonparoxysmal with gradual onset and
gradual termination. SVT from reentry are usually episodic oc-
curring for a few minutes to a few hours and are recurrent. Un-
like SVT from enhanced automaticity, they are rarely incessant,
meaning that the tachycardia rarely persists for 12 hours a day.
AVNRT is generally tolerable except in patients with stenotic
valves, ischemic heart disease, left ventricular (LV) dysfunc-
tion, or cardiomyopathy. In these patients, hypotension or
symptoms of low cardiac output, myocardial ischemia, heart
failure, or actual syncope may occur during tachycardia. It can
also cause symptoms even among healthy patients when the
tachycardia is unusually rapid; thus, syncope can occur when
the tachycardia starts abruptly with a very fast rate or termi-
nates with a very long pause because of overdrive suppression
of the sinus node. The latter occurs when the tachycardia is
associated with sinus node dysfunction. It is rarely associated
with mortality or morbidity in otherwise healthy individuals.
Although physical examination is usually not helpful in the
diagnosis of SVT, prominent neck vein pulsations are often
present and may be the patients chief complaint during
tachycardia. These neck vein pulsations are due to cannon A
waves, which occur when atrial contraction is simultaneous
with ventricular contraction due to retrograde P waves oc-
curring within or immediately after the QRS complex. The
tachycardia causes atrial stretch, which may be followed by a
period of diuresis due to release of atrial natriuretic peptide.
Acute Treatment
Unless the patient is severely hypotensive or in cardiogenic
shock, immediate electrical cardioversion is rarely necessary
in patients with AVNRT because the tachycardia is well toler-
ated. Vagal maneuvers and pharmacologic therapy are usu-
ally very effective in terminating the tachycardia.
Vagal maneuvers: Vagal stimulation should be attempted
as the initial therapeutic maneuver before any pharmaco-
logic agent is given. The ECG should be recorded when vagal
stimulation is performed because vagal stimulation is not
only effective in terminating the tachycardia, but is also help-
ful as a diagnostic maneuver if the tachycardia turns out to be
due to other arrhythmias.
Supraventricular Tachycardia due to Reentry 195
Carotid sinus pressure: The most commonly used and
most effective vagal maneuver in terminating SVT is
carotid sinus pressure. Carotid sinus pressure is always
performed under cardiac monitoring in the recumbent
position. With the neck hyperextended, the common
carotid artery is identified by its pulsations and followed
distally as close to the mandible as possible, usually at the
angle of the jaw where the artery bifurcates into external
and internal carotid arteries. It is at this bifurcation where
the carotid sinus is located. Carotid sinus pressure is per-
formed by applying gentle but constant pressure to the
pulsating artery using both middle and index fingers. Pres-
sure should be applied initially only for a few seconds un-
til slowing of the heart rate can be identified in the cardiac
monitor. The maneuver can be repeated several more
times by pressing the artery at longer intervals if needed,
especially if the previous maneuvers are unsuccessful in
eliciting any response. There is no need to rub or massage
the artery or press the pulsating artery for longer than
5 seconds at a time. Constant gentle pressure on the artery
is all that is necessary. Only one artery should be pressed at
any time. If there is no response, the same maneuver
should be tried on the other carotid artery. This maneuver
can also be repeated if the SVT persists after a pharmaco-
logic agent has been given, but is not effective in terminat-
ing the tachycardia. Occasionally, a tachycardia that is
previously unresponsive to carotid sinus pressure may be-
come more responsive after an intravenous medication
such as calcium channel blocker or digoxin has been given.
If carotid stenosis is suspected by the presence of a carotid
bruit, carotid sinus pressure should not be attempted.
Pharyngeal stimulation: A tongue blade is positioned
at the back of the tongue as if performing a routine
oropharyngeal examination. The tongue blade is gently
brushed to the pharynx to make the patient gag.
Valsalva maneuver: This can be performed by several
methods. The simplest is to instruct the patient to tense the
abdominal muscles by exhaling forcefully against a closed
glottis. The examiner can also make a fist, which is gently
placed on the patients abdomen. The patient, who is re-
cumbent, is instructed to resist by tensing the abdominal
muscles as the examiners fist is gently pressed on the ab-
domen. The procedure can also be performed by blowing
forcefully through a spirometer, balloon, or brown bag.
This can also be done by straining, as if the patient is lifting
a heavy object. The patient, who is recumbent, is asked to
cross both legs on top of one another and instructed to lift
them together while resistance is being applied to prevent
the legs from being lifted. The Valsalva maneuver should
not be performed if the patient is severely hypertensive, in
congestive failure, or if an acute coronary event is suspected
or patient is hemodynamically unstable.
Forceful coughing.
Diving reflex: When the face comes in contact with cold
water, bradycardia usually occurs and is known as the diving
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196 Chapter 16
reflex. This can be done at bedside by immersing the face
in iced water.
Ocular pressure: This vagal maneuver is not recom-
mended since retinal detachment may occur as a poten-
tial complication of the procedure especially if done
forcefully.
Pharmacologic therapy: ABCD are the drugs of choice for
the treatment of AVNRT. (A, adenosine; B, beta blockers; C,
calcium channel blockers; D, digoxin). These drugs are not
necessarily given in alphabetical order.
Adenosine: If vagal maneuvers are not successful in termi-
nating the tachycardia, adenosine is the drug of choice for
terminating AVNRT.
Adenosine should not be given if the patient has bron-
chospastic pulmonary disease because adenosine can pre-
cipitate asthma.
The initial dose of adenosine is 6 mg given as an intravenous
bolus. The injection should be given rapidly within 1 to 2
seconds preferably to a proximal vein followed by a saline
flush. If a peripheral vein is used, the arm where the injec-
tion was given should be immediately raised. If the arrhyth-
mia has not converted to normal sinus rhythm, another bo-
lus using a bigger dose of 12 mg is given IV. A third and final
dose of 12 mg may be repeated if the tachycardia has not re-
sponded to the two previous doses. Approximately 60% of
patients with AVNRT will convert with the first dose within
1 minute and up to 92% after a 12-mg dose.
Adenosine is very effective in terminating AVNRT, but is
also helpful in the diagnosis of other arrhythmias espe-
cially atrial flutter with 2:1 block. A 12-lead ECG or a
rhythm strip should be recorded when adenosine is in-
jected. When adenosine converts AVNRT to normal sinus
rhythm, the tachycardia ends with a retrograde P wave,
implying that the tachycardia was blocked at the slow
pathway, which is usually the most vulnerable part of the
reentrant circuit. The response of AVRT to adenosine is
similar, ending with a retrograde P wave because both
tachycardias are AV nodedependent. Focal atrial tachy-
cardia is not AV nodedependent, although it may re-
spond to adenosine. When focal atrial tachycardia termi-
nates, the tachycardia ends with a QRS complex rather
than a P wave. Atrial flutter with 2:1 block will not re-
spond to adenosine, but will slow the ventricular rate sig-
nificantly allowing the diagnosis of atrial flutter to be-
come obvious by the presence of a regular sawtooth, wavy
undulating baseline between the QRS complexes.
Adenosine is potentiated by dipyridamole, since dipyri-
damole prevents the metabolic breakdown of adenosine. It
is also potentiated by carbamazepine, which may result in
prolonged asystole on conversion of the tachycardia to nor-
mal sinus rhythm. If the patient is taking dipyridamole or
carbamazepine, the initial dose should be cut in half to 3 mg.
Theophylline is the antidote for adenosine. If the patient
is on theophylline, higher doses of adenosine may be
given to treat the SVT if there is no history of bron-
chospastic pulmonary disease. If the patient has reactive
airway disease, adenosine can cause bronchospasm.
If the SVT has not responded after three doses of adenosine
or if adenosine is contraindicated, another pharmacologic
agent should be tried. The choice of the next pharmacologic
agent will depend on the presence or absence of LV dysfunc-
tion or clinical congestive heart failure.
Preserved LV function
n Calcium channel clockers: In patients with preserved
LV function, the next drug of choice after failure to ter-
minate AVNRT with adenosine is verapamil or dilti-
azem. If the patient is not hypotensive, 2.5 to 5 mg of
verapamil is given IV slowly over 2 minutes under
careful ECG and blood pressure monitoring. If there is
no response and the patient remains stable, additional
doses of 5 to 10 mg may be given every 15 to 30 min-
utes until a total dose of 20 mg is given. Alternate dos-
ing with verapamil is to give 5 mg boluses every 15
minutes not to exceed 30 mg. Verapamil is effective in
up to 90% of patients. Verapamil is a hypotensive and
negatively inotropic agent and should not be given
when there is congestive heart failure or LV dysfunc-
tion. Diltiazem is another calcium channel blocker that
can be given at an initial dose of 0.25 mg per kg (equiv-
alent to approximately 15 to 20 mg in a 70-kg patient)
over 2 minutes. If the tachycardia has not terminated
with the first bolus, a higher dose of 0.35 mg/kg or 25
mg is given after 15 minutes. This is followed by a
maintenance IV dose of 5 to 15 mg/hour if needed.
Diltiazem is shorter acting and less hypotensive than
verapamil and may be better tolerated in some pa-
tients. In patients who become hypotensive with vera-
pamil or diltiazem, calcium gluconate or calcium chlo-
ride 5% 10 mL may be given intravenously to reverse
the hypotension. For more detailed dosing of vera-
pamil or diltiazem, see Appendix.
n Beta Blockers: Beta blockers (metoprolol, atenolol,
propranolol, or esmolol) may be tried if the patient
has not responded to the above therapy. Beta blockers
should not be given when there is congestive heart
failure or evidence of LV systolic dysfunction, hy-
potension, or bronchospastic pulmonary disease.
n Metoprolol is given intravenously slowly at a dose of
5 mg and repeated two more times every 5 minutes
if necessary for a total dose of 15 mg in 15 minutes.
n Atenolol is given IV slowly 5 mg over 5 minutes
and repeated once after 10 minutes if needed if the
first dose was well tolerated.
n Propranolol is given at a dose of 0.1 mg/kg. The drug
is given IV slowly not to exceed 1 mg per minute
until the arrhythmia is terminated. A second dose
may be repeated after 2 minutes if needed.
n Esmolol is given at an initial dose of 0.5 mg/kg in-
fused over a minute. This is followed by a mainte-
nance infusion of 0.05 mg/kg/min for the next 4
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minutes (see Appendix for further dosing). If im-
mediate control of SVT is necessary intraopera-
tively, a higher dose of 1 mg/kg may be given over
30 seconds followed by 150 mcg/kg/min mainte-
nance infusion.
n Digoxin: Digoxin has a slow onset of action and is not
as effective as the previously discussed agents. The ini-
tial dose of digoxin in a patient who is not on oral
digoxin is 0.5 mg given slowly IV for 5 minutes or
longer. Subsequent doses of 0.25 mg IV should be
given after 4 hours and repeated if needed for a total
dose of no more than 1.5 mg over a 24-hour period.
n Other Agents:
n Other antiarrhythmic agents that should be con-
sidered include type IA (procainamide), type IC
(propafenone), or type III agents (amiodarone,
ibutilide). The use of these agents requires expert
consultation. These agents should be considered
only if the SVT is resistant to the above pharmaco-
logic agents. For more detailed dosing of these
agents, see Appendix.
n An old remedy, now seldom used, that should be
considered when there is hypotension is acute ele-
vation of systolic blood pressure with arterial vaso-
pressors such as phenylephrine. Intravenous vaso-
pressors may cause bradycardia and AV block by
reflex vagal stimulation of baroreceptors in the
carotid sinus. This may be considered when the pa-
tient is hypotensive but not when there is heart
failure. The initial dose of phenylephrine is 100
mcg given as an IV bolus over 20 to 30 seconds and
repeated in increments of 100 to 200 mcg. A total
dose of 100 to 500 mcg is usually given, usual dose
200 mcg. The maximal dose depends on the blood
pressure response, which should not exceed an ar-
bitrary level of 180 mm Hg systolic.
n Electrical cardioversion: In stable patients, synchro-
nized electrical cardioversion is not encouraged. It
should be attempted only as a last resort.
Presence of heart failure or LV systolic dysfunction
(ejection fraction 40%).
n Digoxin: Although digoxin may not be the most effec-
tive agent, it is the preferred agent when there is LV
dysfunction, decompensated congestive heart failure,
or hypotension. If the patient is not on oral digoxin,
0.5 mg is given intravenously as described previously.
n Other agents: Nondihydropyridine calcium channel
blockers (diltiazem or verapamil) should not be given
when there is decompensated heart failure or LV dys-
function. Verapamil is contraindicated because it is
negatively inotropic and has a longer half-life than dil-
tiazem. Diltiazem may be more tolerable because of its
shorter half-life and may be tried unless there is de-
compensated heart failure. The drug is given IV slowly
at an initial dose of 15 to 20 mg (0.25 mg/kg).
Supraventricular Tachycardia due to Reentry 197
Intravenous beta blockers (metoprolol, atenolol, pro-
pranolol, esmolol) should not be given in the presence
of LV dysfunction, heart failure, or bronchospastic
pulmonary disease. Although beta blockers are indi-
cated as long-term therapy for chronic congestive
heart failure from systolic LV dysfunction, they are
given orally in small doses and titrated slowly over
several days. They should not be given in intravenous
doses such as those used for the emergency treatment
of SVT with preserved systolic LV function.
n Antiarrhythmic agents: Amiodarone, a Class III
agent, may be the only intravenous antiarrhythmic
drug that may be tried when there is LV dysfunction.
This agent, however, should be considered only if the
SVT has not responded to the other agents.
n Electrical cardioversion: Synchronized electrical car-
dioversion is rarely necessary and should be at-
tempted only as a last resort.
Long-term therapy: Long-term oral therapy is generally
given to prevent further recurrence of the arrhythmia, mini-
mize symptoms, and improve quality of life rather than to
prolong survival.
For patients with minimal or no symptoms during tachy-
cardia, especially if the arrhythmia occurs only infre-
quently, no oral medications are needed.
For patients who develop symptoms of hemodynamic in-
stability during AVNRT or those with recurrent and pro-
longed arrhythmias, chronic oral medical therapy may be
tried. In patients without LV dysfunction, oral medications
include calcium channel blockers (verapamil or diltiazem),
beta blockers (atenolol, metoprolol, or propranolol), or
digoxin. Although digoxin is less effective than the other
agents, it may be the only oral agent that is appropriate for
long-term maintenance therapy in patients with LV dys-
function. Beta blockers, such as carvedilol and metoprolol
succinate, are standard agents for the treatment of systolic
LV dysfunction and should be titrated slowly orally until an
adequate maintenance dose is given that is also effective for
controlling or preventing the tachycardia.
Catheter ablation of the reentrant circuit with a chance of
permanent cure should be considered in patients who do
not respond to medical therapy or those not willing to
take oral medications. The success rate of catheter abla-
tion is approximately 96% with a recurrence rate of 3% to
7% after successful ablation. Because the reentrant circuit
is close to the AV node, there is a 1% or more chance of
developing second- or third-degree AV block, which may
require implantation of a permanent pacemaker.
Prognosis
Because most AVNRT occurs in young patients with struc-
turally normal hearts, the tachycardia is usually tolerable and
overall prognosis is excellent with a chance of permanent cure
among patients who are willing to undergo electrical ablation.
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198 Chapter 16

Atrial Impulse Atrial Impulse

Figure 16.16: Orthodromic and enters bypass tract
enters AV node
Antidromic Atrioventricular Reen-
trant Tachycardia (AVRT). Bypass tract
In orthodromic AVRT (A), the QRS com-
plexes are narrow since the ventricles
are activated through the normal AV QRS complexes are
conduction system. In antidromic AVRT narrow since the QRS complexes are
ventricles are activated wide since ventricles
(B), the QRS complexes are wide
through the AV node are activated through
because the ventricles are activated the bypass tract
through the bypass tract.

A. Orthodromic AVRT B. Antidromic AVRT

tract, the QRS complex will be narrow. This type of

Atrioventricular Reciprocating
Tachycardia
AVRT: AVRT is the second most common SVT occur-
ring in approximately 30% of all reentrant SVT. This
type of SVT is associated with a bypass tract that con-
nects the atrium directly to the ventricle.
Normally, an atrial impulse can conduct to the ventricles
only through the AV node. When a bypass tract is pres-
ent, a second pathway is created for reentry to occur.
Thus, an atrial impulse can enter the ventricles through
the AV node and return to the atria through the bypass
tract (Fig. 16.16A) or enter the ventricle through the by-
pass tract and return to the atria through the AV node
(Fig. 16.16B).
AVRT may have narrow or wide QRS complexes:
AVRT with narrow QRS complexes: When the
atrial impulse enters the ventricles through the AV
node and returns to the atria through the bypass
tachycardia is called orthodromic AVRT (Fig. 16.16A).
AVRT with wide QRS complexes: When the atrial
impulse enters the ventricles through the bypass
tract and returns to the atria through the AV node,
the QRS complex will be wide. This type of tachy-
cardia is called antidromic AVRT (Fig. 16.16B). An-
tidromic AVRT is an example of SVT with wide QRS
complexes and will be further discussed in Chapter
20, Wolff-Parkinson-White Syndrome.
Mechanism: AVRT with narrow QRS complexes is
triggered by a premature impulse originating from the
atria or ventricles. The diagram below illustrates how
the tachycardia is initiated by a premature atrial com-
plex (PAC) (Fig. 16.17).
The PAC should be perfectly timed to occur when
the AV node (the slow pathway) has fully recovered,
while the bypass tract (the fast pathway) is still re-
fractory from the previous impulse. Because the AV
node has a shorter refractory period, the premature

Figure 16.17: Mechanism of Narrow

Complex Atrioventricular Reentrant
Tachycardia (AVRT). The diagram
shows how a narrow complex AVRT is initi- (#1) Premature Atria
ated by a premature atrial complex (PAC). atrial complex (#5) Impulse activates
The PAC finds the bypass tract still enters the AV PAC atria retrogradely and
node but not reenters AV node
refractory because of its longer refractory
the bypass
period but is conducted through the AV tract
node, which has a shorter refractory period,
(#4) Impulse
resulting in AVRT with narrow QRS enters bypass
complexes (see text). (#2) The impulse is tract from
conducted through ventricles to
the AV node slowly atrium

(#3) Both ventricles

are activated
synchronously
Ventricles
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atrial impulse will enter the AV node but not the by-
pass tract (Fig. 16.17, #1).
The impulse conducts slowly through the AV node
(#2) and activates the ventricles normally resulting in
a narrow QRS complex (#3). After the ventricles are
activated, the impulse circles back through the bypass
tract (#4) and activates the atria retrogradely (#5).
After the atria are activated, the impulse can again
enter the AV node and the circuit starts all over again.
In AVRT, the reentrant circuit involves a large mass of
tissue consisting of the atria, AV node, bundle of His,
bundle branches and fascicles, ventricles, and bypass
tract before returning to the atria. AVRT therefore is a
form of macro-reentry.
ECG Findings: Narrow complex AVRT has the follow-
ing features:
The atria and ventricles are essential components of
the circuit; thus, activation of the atria and ventri-
cles cannot be simultaneous. The P wave, therefore,
cannot be buried within the QRS complex. It should
always be inscribed outside the QRS complexes.
Because the atria are activated from the bypass tract,
the P waves are inscribed retrogradely. The P waves
are usually inverted in II, III, and aVF although the
configuration of the P wave may vary depending on
the location of the bypass tract.
Typically, the retrograde P waves are inscribed im-
mediately after the QRS complexes and deform the
ST segments. Thus, the R-P interval is shorter than
the PR interval (Fig. 16.18). This is the typical or
most common presentation of AVRT.
AV block is not possible during AVRT because the
atria and ventricles are essential components of the
circuit; thus, every retrograde P wave is always fol-
lowed by a QRS complex during tachycardia. When
AV block occurs, the reentrant circuit (and therefore
the tachycardia) will terminate.
An example of AVRT is shown in Figure 16.19. Note
that the P waves are retrograde and are inverted in leads
II, III, and aVF and also in V4 to V6. The retrograde P
Leads II, III or aVF
Retrograde P wave is closer to the
previous QRS Comple
R-P Interval shorter
Supraventricular Tachycardia due to Reentry 199
wave is inscribed immediately after the QRS complex,
deforming the ST segment of the previous QRS complex
with an R-P interval that is shorter than the PR interval.
Other examples of narrow complex tachycardia with
retrograde P waves immediately after the QRS complex
are shown in Figs. 16.20 to 16.22. The retrograde P
waves may be mistaken for inverted T waves.
There are two types of narrow complex (orthodromic)
AVRT: typical and atypical (see Figs. 16.22 to 16.25).
Typical AVRT: AVRT is typical when the retrograde P
waves are inscribed immediately after the QRS com-
plex and deform the ST segment or T wave of the pre-
ceding complex (Figs. 16.21 and 16.22). Conduction
from ventricle to atrium across the bypass tract (R-P
interval) is faster than conduction from atrium to
ventricle across the AV node (PR interval); thus, the
R-P interval is shorter than the PR interval. In typical
AVRT, the AV node is the slow pathway and the by-
pass tract is the fast pathway (slow/fast activation).
Virtually all cases of AVRT present in this manner.
Atypical AVRT: AVRT is atypical when the retro-
grade P waves occur in front of the QRS complexes
(Fig. 16.23); thus, the R-P interval is longer than the
PR interval. Atypical AVRT is associated with a
slowly conducting bypass tract. Conduction from
ventricle to atrium across the bypass tract (R-P in-
terval) is slower than conduction from atrium to
ventricle (PR interval) across the AV node (fast/slow
activation). This type of AVRT is rare. The ECG of
atypical AVRT is similar to that of atypical AVNRT.
Typical AVRT versus AVNRT: When retrograde P
waves are inscribed immediately after the QRS com-
plexes during tachycardia, AVRT may be difficult to dif-
ferentiate from AVNRT (Fig. 16.24). One clue in differ-
entiating AVRT from AVNRT is the duration of the R-P
interval (Figs. 16.21 and 16.22A). The R-P interval in
AVRT should measure 80 milliseconds in the surface
ECG because this is the minimum time required for the
impulse to travel from ventricles to atria across the by-
pass tract. If the retrograde P wave is too close to the QRS
complex and the R-P interval is 80 milliseconds, as
Figure 16.18: Typical Atrioventric-
ular Reentrant Tachycardia
(AVRT). In AVRT, the retrograde P
wave is inscribed immediately after the
QRS complex with the R-P interval
shorter than the PR interval.This is the
typical or most common presentation
of AVRT.
PR Interval longer
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200 Chapter 16

A. During Tachycardia

B. During Normal Sinus Rhythm

Figure 16.19: Twelve-lead Electrocardiogram in Atrioventricular Reentrant Tachycardia (AVRT).

(A) A narrow complex tachycardia with retrograde P waves in II, III, aVF, and in V4 to V6 (arrows). The retrograde P
waves are inscribed after the QRS complexes and deform the ST segments or T waves of the previous complex with
an R-P interval shorter than PR interval. (B) The same patient after conversion to normal sinus rhythm.The
retrograde P waves are no longer present.

shown in Figure 16.22A, AVRT is unlikely and AVNRT
is the more likely diagnosis.
Because the R-P interval in AVRT measure 80 mil-
liseconds, the retrograde P waves are usually inscribed
separately from the QRS complexes, whereas in
AVNRT, the retrograde P waves are usually connected
to the terminal portion of the QRS complexes.
Concealed bypass tract: In 30% to 40% of patients
with AVRT, the bypass tract is concealed, indicating
that the bypass tract is capable of conducting only in a
retrograde fashion from ventricle to atrium but not
from atrium to ventricle (see Chapter 20, Wolff-
Parkinson-White Syndrome). Thus, the baseline ECG
during normal sinus rhythm or upon conversion of the
AVRT to normal sinus rhythm will not show any pre-
excitation (no delta wave or short PR interval). The
presence of a bypass tract is suspected only when
tachycardia from AVRT occur.
Manifest bypass tract: Patients with AVRT with
manifest bypass tracts have preexcitation (delta wave
and short PR interval) in baseline ECG during nor-
mal sinus rhythm. These bypass tracts are capable of
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Supraventricular Tachycardia due to Reentry 201

A. During AVRT

B. During Normal Sinus Rhythm

Figure 16.20: Retrograde P Waves can be Mistaken for Inverted T Waves in Atrioventricular Reen-
trant Tachycardia (AVRT). (A) A 12-lead electrocardiogram (ECG) during tachycardia.The retrograde P wave is in-
scribed immediately after the QRS complex with the R-P interval shorter than the PR interval.This is the most common
presentation of AVRT.The retrograde P waves may be mistaken for inverted T waves in II, III, and aVF (arrows). (B) A 12-
lead ECG of the same patient upon conversion to normal sinus rhythm.The retrograde P waves are no longer present.

Typical AVRT Figure 16.21: The R-P Interval in Typical

Atrioventricular Reentrant Tachycardia
Retrograde P wave (AVRT). In typical AVRT,the R-P interval
(measured from the onset of QRS complex to the
onset of the retrograde P wave) should measure
80 ms.This is the time required for the impulse to
travel from ventricles to atria retrogradely through
the bypass tract. The length of the arrow in (B) indi-
R-P Interval >80 ms >80 ms R-P >80 ms cates the R-P interval,which is the time required for
the impulse to travel from ventricle to atrium across
A B the bypass tract and is 80 ms.ms,milliseconds.
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202 Chapter 16

A B

Figure 16.22: Atrioventricular Nodal Reentrant Tachycardia (AVNRT). (A) Retrograde

P waves are inscribed immediately behind the QRS complexes during tachycardia. Note that
the R-P interval is 80 ms (distance between the two arrows), hence the tachycardia is AVNRT
and not atrioventricular reentrant tachycardia (AVRT). In AVRT, at least 80 ms is required for the
impulse to travel from ventricle to atrium across the bypass tract in the surface electrocardio-
gram. (B) Same patient on conversion to normal sinus rhythm. ms, milliseconds.

Leads II, III or aVF

Retrograde P waves

R-P Interval PR Interval

longer shorter

Atypical AVRT retrograde P waves are in front of the QRS complexes

Figure 16.23: Atypical Atrioventricular Reentrant Tachycardia (AVRT). In atypi-

cal AVRT, the retrograde P waves are inscribed in front of the QRS complexes with the R-P in-
terval longer than PR interval. Atypical AVRT is associated with a slowly conducting bypass
tract resulting in a long R-P interval.

Figure 16.24: Typical Atrioventricular Reentrant Tachycardia (AVRT). Twelve-

lead electrocardiogram showing typical AVRT. Retrograde P waves are present in leads II, III,
and aVF (arrows) with R-P interval measuring 80 milliseconds. The R-P interval is shorter
than the PR interval.
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Supraventricular Tachycardia due to Reentry 203

Figure 16.25: Atypical Atrioventricular Reentrant Tachycardia (AVRT). In atypical AVRT, retrograde P waves
are in front of the QRS complex (R-P interval longer than PR interval) because of the presence of a slowly conducting
bypass tract.The supraventricular tachycardia is terminated by a perfectly timed premature atrial complex (arrow).

conducting from atrium to ventricle and also from ven-
tricle to atrium. This will be discussed more extensively
in Chapter 20, Wolff-Parkinson-White Syndrome.
Electrical alternans: In electrical alternans, the ampli-
tude of the QRS complexes alternates by more than 1
mm. Although electrical alternans is more commonly
seen in AVRT (Fig. 16.26), electrical alternans can also
occur with other types of SVT. Electrical alternans is
more commonly a function of the heart rate rather than
the type or mechanism of the SVT.
Localizing the bypass tract: Most bypass tracts are
located at the free wall of the left ventricle (50% to
60%) followed by the posteroseptal area (20% to 30%),
free wall of the right ventricle (10% to 20%), and the
anteroseptal area (5%). The atrial insertion of the by-
pass tract can be localized by the configuration of the P
wave during AVRT. The bypass tract can also be local-
ized during sinus rhythm if the baseline ECG shows
ventricular preexcitation. This is further discussed in
Chapter 20, Wolff-Parkinson-White Syndrome.

Figure 16.26: Electrical Alternans. In electrical alternans, taller QRS complexes alternate
with shorter QRS complexes by more than 1 mm. Arrows point to a tall QRS complex alternating
with a smaller QRS complex. Electrical alternans is more commonly seen in atrioventricular reen-
trant tachycardia (AVRT) than with other types of supraventricular tachycardia (SVT) because the
ventricular rate of AVRT is generally faster when compared with other types of SVT.
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204 Chapter 16

Figure 16.27: Localizing the Bypass Tract.

If the P waves are inverted in lead I during tachy- Lead I P
cardia (A), the bypass tract is left sided. If the P
waves are upright in lead I during the tachycar-
dia (B), the bypass tract is right sided. Arrows
represent the direction of atrial activation.
Left Sided Bypass Tract: P waves are
negative in Lead I during tachycardia

Lead I P

Right Sided Bypass Tract: P waves are

positive in Lead I during tachycardia

Left-sided bypass tract:If the P waves are inverted in
lead I during tachycardia, the direction of atrial activa-
tion is from left atrium to right atrium. This indicates
that the bypass tract is left sided since the left atrium is
activated earlier than the right atrium (Fig. 16.27A).
Right-sided bypass tract: If the P waves are up-
right in lead I, the direction of atrial activation is
from right atrium to left atrium. Because the right
atrium is activated earlier than the left atrium, the by-
pass tract is right sided (Figs. 16.27B and 16.28).
Localizing the bypass tract: In a patient with known
Wolff-Parkinson-White (WPW) syndrome, rate-related
bundle branch block may occasionally develop during
narrow complex AVRT. If the rate of the tachycardia

A. During Tachycardia
Figure 16.28: Atrioventricular Reentrant
Tachycardia (AVRT). (A) A 12-lead electrocardio-
gram during AVRT. The P waves are inverted in II, III,
and aVF and upright in I and aVL (arrows). Retrograde
P waves are also present in V3 to V5. The presence of
upright P waves in I and aVL during AVRT suggests
that atrial activation is from right to left consistent
with a right sided bypass tract. Note that on conver-
sion to normal sinus rhythm (B), no evidence of pre-
excitation is present. This type of AVRT is associated
with a concealed bypass tract.

B. Normal Sinus Rhythm

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Supraventricular Tachycardia due to Reentry 205

A B C
Atria Atria Atria

Narrow Complex AVRT Rate Related LBBB

(No change in circuit) Rate Related RBBB
(Circuit is longer)

(A) Narrow Complex AVRT (B) Rate Related LBBB (C) Rate Related RBBB
Rate is the same Rate becomes slower

Figure 16.29: Localizing the Bypass Tract. The diagrams explain how a rate-
related bundle branch block will slow down the ventricular rate during AVRT if the
bypass tract is on the same side as the bundle branch block. (A) Narrow complex
AVRT with a right-sided bypass tract. (B) If a rate-related LBBB develops during tachy-
cardia, the circuit is not altered by the bundle branch block and the rate of the tachy-
cardia remains unchanged. (C) If a rate-related right bundle branch block occurs, the
rate of the tachycardia will become slower if the bypass tract is right sided because
the right ventricle and bypass tract have to be activated from the left bundle branch,
resulting in a longer and slower circuit. AVRT, atrioventricular reentrant tachycardia;
LBBB, left bundle branch block; RBBB, right bundle branch block.

becomes slower when the rate-related bundle branch
block occurs, the bypass tract is on the same side as the
bundle branch block. For example:
RBBB: If a rate-related RBBB occurs during tachy-
cardia and the ventricular rate becomes slower, the
bypass tract is right sided (Fig. 16.29).
LBBB: If a rate-related LBBB occurs and the ventric-
ular rate becomes slower during the tachycardia, the
bypass tract is left sided. Conversely, if the heart rate
does not become slower, the bypass tract is at the
opposite side.
ECG Findings of Orthodromic AVRT
1. Orthodromic AVRT is a narrow complex tachycardia with reg-
ular R-R intervals.
2. The P waves and QRS complexes are inscribed separately be-
cause the atria and ventricles are part of the reentrant circuit.
3. The configuration of the retrograde P waves may be different,
depending on the location of the bypass tract. The P waves are
commonly inverted in leads II, III, and aVF because the atria
are activated by the bypass tract from below upward.
4. In typical AVRT, the retrograde P wave may be inscribed at
the ST segment or T wave of the previous complex, thus, the
retrograde P wave is closer to the previous QRS complex
than the next QRS complex (R-P interval is shorter than the
PR interval).
5. In atypical AVRT, the retrograde P waves are inscribed before the
QRS complex and are closer to the next QRS complex than to the
previous QRS complex (R-P interval longer than PR interval).
6. AV block is not possible during tachycardia. AVRT is excluded
if AV block occurs.
7. Electrical alternans favors AVRT but does not exclude other
types of SVT.
Mechanism
AVRT is a reentrant tachycardia associated with a bypass
tract. The bypass tract connects the atrium directly to the
ventricle and provides an alternate route by which the atrial
impulse can conduct anterogradely to the ventricles and the
ventricular impulse retrogradely to the atrium.
The tachycardia is precipitated by an ectopic impulse origi-
nating from the atria or ventricles. The ectopic impulse
should occur when one pathway (either the AV node or by-
pass tract) has fully recovered and the other pathway is still
refractory.
The tachycardia is very regular because the impulse follows a
fixed pathway consisting of the AV node, bundle of His, a bun-
dle branch, ventricle, bypass tract, and atrium. Second-degree
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206 Chapter 16
AV block is not possible since the AV node is an essential
component of the reentrant circuit. If the impulse is blocked
at the AV node, the reentrant circuit will terminate.
The tachycardia may have wide or narrow complexes de-
pending on how the ventricles are activated.
Antidromic AVRT: Antidromic AVRT is associated with
wide QRS complexes. The QRS complex is wide because
the atrial impulse activates the ventricles anterogradely
through the bypass tract. Because the impulse is con-
ducted outside the normal conduction system, the QRS
complexes are wide measuring 0.12 seconds. An-
tidromic AVRT is a classic example of wide complex
tachycardia due to SVT. This type of SVT can be mistaken
for ventricular tachycardia. This is further discussed in
Chapter 20, Wolff-Parkinson-White Syndrome.
Orthodromic AVRT: Orthodromic AVRT is associated
with narrow QRS complexes. The QRS complex is narrow
because the atrial impulse activates the ventricles antero-
gradely through the AV node. Because the ventricles are
activated normally, the QRS complexes are narrow meas-
uring 0.12 seconds. Orthodromic AVRT can be typical
or atypical.
n Typical AVRT: The P waves deform the ST segment or
early portion of the T wave of the previous complex,
thus the R-P interval is shorter than the PR interval. In
typical AVRT, the AV node is the slow pathway and the
bypass tract the fast pathway (slow/fast activation).
n Atypical AVRT: The P waves precede the QRS com-
plexes, thus, the R-P interval is longer than the PR in-
terval. In atypical AVRT, the AV node is the fast path-
way and the bypass tract the slow pathway (fast/slow
activation). This type of AVRT is rare.
Clinical Significance
AVRT is the second most common SVT, occurring in ap-
proximately 30% of all reentrant SVT. It is another classic ex-
ample of a tachycardia that is paroxysmal with abrupt onset
and abrupt termination.
The bypass tract may be capable of conducting only retro-
gradely (ventricle to atrium) but not anterogradely
(atrium to ventricle). Such bypass tracts are called con-
cealed bypass tracts. When the bypass tract is concealed,
preexcitation (presence of short PR interval and delta
wave) is not present in the 12-lead ECG during normal si-
nus rhythm. Patients with AVRT with preexcitation during
normal sinus rhythm have manifest bypass tracts. These
patients with preexcitation and symptoms of tachycardia
have WPW syndrome.
The location of the bypass tract can be diagnosed by the
morphology of the P waves during SVT.
If the bypass tract is left sided, activation of the left atrium
occurs earlier than the right atrium resulting in inverted P
waves in lead I during the tachycardia.
If the bypass tract is right sided, the right atrium is acti-
vated before the left atrium, resulting in upright P waves
in lead I during the tachycardia.
When a rate-related bundle branch block occurs and the
rate of the tachycardia slows down, the bypass tract is on the
same side as the bundle branch block. Thus, if rate-related
RBBB occurs and the rate of the tachycardia is slower, the
bypass tract is right sided. If LBBB occurs and the rate of
the tachycardia is slower, the bypass tract is left sided.
Atypical AVRT: Although AVRT is almost always precipi-
tated by an ectopic impulse, there is a subset of atypical
AVRT in which the tachycardia may occur spontaneously
during an abrupt onset of sinus tachycardiasuch as dur-
ing exertion, excitement, or enhanced sympathetic activity.
This type of SVT should be recognized because it is usually
incessant (the tachycardia lasts more than 12 hours per day)
and may result in tachycardia mediated cardiomyopathy.
This type of tachycardia is also called permanent junctional
reciprocating tachycardia or PJRT. The tachycardia is asso-
ciated with a slowly conducting bypass tract; thus, the P
waves are in front of the QRS complex with R-P interval
longer than PR interval. The bypass tract is located at the
posteroseptal area very close to the orifice of the coronary
sinus and may be treated successfully with radiofrequency
ablation. The tachycardia is usually poorly responsive to
medical therapy.
Because the retrograde P waves occur at the ST segment or T
waves during tachycardia, contraction of the atria occurs
during systole when the mitral and tricuspid valves are
closed. This can cause cannon A waves, which are prominent
jugular neck vein pulsations during tachycardia. The pres-
ence of cannon A waves in the neck during SVT suggests
AVNRT or AVRT as the cause of the tachycardia.
Acute Treatment
The acute treatment of narrow complex AVRT is identical to
that of AVNRT (see Treatment of AVNRT). Because AVRT is
dependent on the AV node for perpetuation of the arrhyth-
mia, treatment includes vagal maneuvers and pharmacologic
agents that block the AV node. Similar to AVNRT, adenosine
given intravenously is the drug of choice to terminate the
tachycardia. The tachycardia ends with a retrograde P wave,
meaning that the last part of the tachycardia to be recorded
before the rhythm becomes sinus is a retrograde P wave. This
implies that the tachycardia was blocked at the level of the
AV node, regardless whether the AV node is a fast or slow
pathway. Similar to adenosine, AV nodal blockers such as
verapamil and diltiazem terminate the tachycardia at the
level of the AV node causing a P wave to be inscribed last,
before the rhythm converts to normal sinus.
Although adenosine is the drug of choice among patients
with paroxysmal SVT, adenosine can precipitate asthma and
should not be given to patients with history of severe reactive
airway disease. Some of these patients with asthma may
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A. Diagrammatic Representation of SART
Lead II
1 have SART.The SART can be terminated (arrow 1) or
B. Lead II Rhythm Strip
already be on theophylline, which is the antidote for adeno-
sine. Adenosine is less effective for the treatment of SVT in
patients who are already on theophylline.
Adenosine can potentially cause atrial fibrillation in 1% to
10% of patients. This can result in potential lethal complica-
tion among patients with AVRT with manifest bypass tracts
(preexcitation or WPW pattern is present in baseline ECG).
Atrial fibrillation in these patients can result in very rapid
ventricular responses, which can result in hemodynamic col-
lapse. This complication should be anticipated when treating
AVRT so that a defibrillator is available if needed.
Prognosis
The prognosis of patients with orthodromic AVRT with con-
cealed bypass tracts (no evidence of preexcitation in baseline
ECG) is good. Similar to AVNRT, the arrhythmia can be per-
manently cured with electrical ablation. Patients should be
referred to a facility with extensive experience. Early referral
should be done if the tachycardia is recurrent or the patient
cannot tolerate medications.
Patients with evidence of preexcitation during normal sinus
rhythm may have a different prognosis (see Chapter 20,
Wolff-Parkinson-White Syndrome). These patients may de-
velop atrial fibrillation as a complication of the SVT and
therefore can potentially develop arrhythmias that are more
lethal. These patients with manifest bypass tracts and known
WPW syndrome should be referred to an electrophysiologist
for further evaluation.
Other Types of SVT from Reentry
There are two other types of SVT due to reentry: sinoa-
trial reentrant tachycardia (SART) and intra-atrial
reentrant tachycardia (IART). These two types of reen-
trant SVT are relatively uncommon.
Supraventricular Tachycardia due to Reentry 207
Figure 16.30: Sinoatrial Reentrant Tachycar-
dia (SART). (A) Diagrammatic representation of
SART. Because the sinus node is part of the
reentrant circuit, the P waves resemble sinus tachy-
cardia and are upright in leads II, III, and aVF. (B) Con-
tinuous lead II rhythm strip of a patient thought to
precipitated (arrow 2) by premature atrial
complexes and is paroxysmal.
SART: SART is a type of micro-reentrant tachycardia
involving the sinus node and contiguous atrium. The
tachycardia is difficult to differentiate from sinus tachy-
cardia because the sinus node is part of the reentrant
circuit. During tachycardia, the P waves are identical to
sinus P waves (Figs. 16.30 and 16.31) and easily mis-
taken for sinus tachycardia.
The tachycardia is usually precipitated and terminated by
a premature atrial impulse and is therefore paroxysmal
with an abrupt onset and abrupt termination (Fig.
16.30). This is in contrast to sinus tachycardia, which has
a slow onset and gradual termination and is nonparoxys-
mal. SART can also be terminated by vagal maneuvers as
well as agents that block the AV node because AV nodal
blocking agents also inhibit the sinus node. This includes
adenosine, beta blockers, calcium blockers, and digoxin.
Figure 16.31A,B show the difficulty in making a diag-
nosis of SART. Except for the abrupt onset and termi-
nation, the tachycardia is identical and easily mistaken
for sinus tachycardia.
ECG Findings of SART
1. The ECG of SART is identical to that of sinus tachycardia. The
P waves precede the QRS complexes and are upright in leads I,
II, and aVF.
2. The tachycardia is paroxysmal with abrupt onset and ter-
mination.
3. It is usually precipitated and can be terminated by premature
atrial complexes.
4. The atrial rate is usually not very rapid and is usually 120 to
150 bpm but can be 100 bpm.
Mechanism
SART is another example of microreentry. The reentrant
SVT includes the sinus node and surrounding atrial tissue.
Because the sinus node is part of the reentrant pathway, the
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208 Chapter 16

A. During SART
Figure 16.31: Twelve-lead Electrocardio-
gram of Sinoatrial Reentrant Tachycardia
(SART). (A, B) From the same patient. (A) A 12-ead
electrocardiogram (ECG) during SART. (B) A 12-lead
ECG immediately on conversion of the SART to nor-
mal sinus rhythm. Note that the P waves are
virtually identical during tachycardia and during
normal sinus rhythm. Most patients with SART are
difficult to diagnose because the tachycardia is eas-
ily mistaken for sinus tachycardia.

B. During normal sinus rhythm

P waves during tachycardia resemble sinus P waves and may
be difficult to differentiate from sinus tachycardia. Unlike si-
nus tachycardia, ectopic atrial impulses can terminate or pre-
cipitate SART. SART can also be precipitated or terminated
by programmed electrical stimulation of the atrium similar
to the other reentrant tachycardia and is paroxysmal with
abrupt onset and abrupt termination. This is in contrast to
sinus tachycardia, which is nonparoxysmal.
including adenosine, beta blockers, calcium channel blockers,
and digoxin because these agents also inhibit the sinus node.
In symptomatic patients, long-term therapy is usually effec-
tive in preventing recurrences. This may include oral beta
blockers, nondihydropyridine calcium channel blockers such
as diltiazem and verapamil, and digoxin.
Sinus node modification using radiofrequency ablation is of-
ten useful if the tachycardia is intractable to medications.

Clinical Implications Prognosis

SART is uncommon, occurring in 5% of all reentrant SVT.
SART is usually associated with structural cardiac disease.
SART is difficult to differentiate from sinus tachycardia. Be-
cause SART involves the sinus node as part of the reentrant
circuit, the morphology of the P waves resemble sinus tachy-
cardia and are upright in leads I, II, and aVF.
The tachycardia can cause symptoms of lightheadedness but
usually not syncope because the atrial rate is usually 120 to
150 bpm, rarely exceeds 180 bpm and can be slower than 100
bpm. P waves precede each QRS complex; thus, atrial contri-
bution to LV filling is preserved during tachycardia.
Acute Treatment
Appropriate therapy is usually not instituted early because
the tachycardia is easily mistaken for sinus tachycardia,
which is a physiologic response to a variety of clinical situa-
tions. Because the sinus node is part of the reentrant circuit,
it can be terminated by vagal maneuvers such as carotid sinus
stimulation. It can also be terminated by AV nodal blockers
SART is usually well tolerated and therapy is given primarily
to improve symptoms and prevent recurrence of the tachy-
cardia. Because SART is associated with structural cardiac
disease, prognosis will depend primarily on the underlying
cardiac condition.
IART
Intraatrial Reentrant Tachycardia: IART is another
SVT due to reentry. The electrical circuit is confined to a
small area in the atrium and therefore is a form of micro-
reentry (Fig. 16.32). The reentrant circuit may be larger if
it circles around a scar tissue or around a healed surgical
incision such as a previous atrial septal defect repair.
The tachycardia starts from a focal area and spreads
circumferentially to activate the whole atria. The mor-
phology of the P wave will depend on the origin of the
tachycardia; thus, the P wave may be upright, inverted,
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Lead aVL
Sinus
Node A
Atria
Lead aVL
B
C Leads II, III and aVF
Atria
Figure 16.32: Intraatrial Reentrant Tachycardia
(IART). In IART, a micro-reentrant circuit is present in the
atrium, which spreads circumferentially to activate the whole
atria. IART is therefore included as an example of focal atrial
tachycardia.The morphology of the P wave will depend on the
origin of the tachycardia. (A) The P waves are upright or biphasic
in lead aVL because the reentrant circuit originates from the
right atrium close to the sinus node. (B) The P waves are inverted
in lead aVL because the impulse originates from the left atrium.
(C) The P waves are inverted in lead II, III, and aVF because the
tachycardia originates from the bottom of the atria (see also
Figs. 13.6 and 13.7).
or biphasic in lead II. Because the tachycardia origi-
nates from the atria, the P waves are inscribed before
the QRS complexes with a PR interval 0.12 seconds.
Atrial tachycardia from IART is difficult to distinguish
from atrial tachycardia resulting from enhanced or
triggered automaticity using the surface ECG. Because
these tachycardias all look alike electrocardiographi-
cally, they are all included as examples of focal atrial
tachycardia regardless of the mechanism and will be
further discussed in Chapter 17, Supraventricular
Tachycardia due to Altered Automaticity.
ECG Findings of IART
1. The P waves are uniform in configuration and precede each
QRS complex with a rate of 110 to 200 bpm.
2. The configuration of the P waves depends on the origin of the
tachycardia and may be upright, biphasic or inverted in leads
II, III, or aVF.
3. The atrial impulse is conducted to the ventricles through the
normal AV conduction system; thus, the PR interval is usually
0.12 seconds. Because the tachycardia is not dependent on
the AV node, AV block can occur.
Mechanism
IART is another example of microreentry within the atria.
The reentrant circuit may be confined to a small area in the
atrium because of inflammation, scarring, or previous sur-
Supraventricular Tachycardia due to Reentry 209
gery. The impulse spreads circumferentially until the whole
atria are activated. The P waves are uniform in configuration
since the impulse originates from a focal area in the atria.
The P waves precede each QRS complex with PR interval
shorter than R-P interval.
Clinical Significance, Treatment,
and Prognosis
Although IART is an example of reentrant tachycardia, the
ECG findings cannot be differentiated from other types of
atrial tachycardia because of enhanced or triggered automatic-
ity. Thus IART is included as an example of focal atrial tachy-
cardia. The clinical significance, treatment, and prognosis of
focal atrial tachycardia will be further discussed in Chpater 17,
Supraventricular Tachycardia due to Altered Automaticity,
under Focal Atrial Tachycardia.
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Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
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the Management of Patients With Supraventricular Arrhyth-
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Waldo AL, Biblo LA. Atrioventricular nodal-independent
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2002:14531478.
Waxman MB, Wald RW, Sharma AD, et al. Vagal techniques for
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Supraventricular Tachycardia
due to Altered Automaticity
Introduction
Other mechanisms by which supraventricular tachy-
cardia (SVT) can occur include enhanced automaticity
and triggered activity.
SVT from enhanced automaticity: Unlike reentrant
SVT, which is dependent on the presence of a reentrant
circuit, SVT from enhanced automaticity is dependent
on cells with automatic properties. Cells with pacemak-
ing properties exhibit diastolic depolarization character-
ized by a slowly rising slope during phase 4 of the action
potential. Once threshold potential is reached, the cells
discharge automatically. This is in contrast to non-pace-
making cells, in which phase 4 is flat and therefore the
resting potential never reaches threshold (Fig. 17.1A, B).
Examples of cells with automatic properties are cells
within the sinus node, atrioventricular (AV) junc-
tion, and throughout the AV conduction system ex-
cept the midportion of the AV node. Although the
cells of the AV conduction system have automatic
properties and are capable of discharging sponta-
neously, their rate of discharge is slower than that of
the sinus node. These cells therefore are depolarized
17
by the propagated sinus impulse and serve as backup
or latent pacemakers.
Ordinary working myocytes in the atria and ventricles
do not exhibit phase 4 diastolic depolarization, but
may develop this property when they become patho-
logic, as would occur during ischemia or injury.
The following types of SVT are due to enhanced auto-
maticity (see Figure 17.2):
Pathologic sinus tachycardia: This tachycardia is
due to enhanced automaticity of the sinus node cells
and may be clinically difficult to differentiate from
physiologic sinus tachycardia (Fig. 17.2A).
Atrial tachycardia: The atria, including the atrial
appendage, large veins draining into the atria (pul-
monary veins, vena cava, and coronary sinus) or even
the mitral or tricuspid annulus, may contain cells
with properties of automaticity. The rate of discharge
of these cells may be enhanced, resulting in atrial
tachycardia. The tachycardia may be unifocal or focal
(Fig. 17.2B) or it may be multifocal (Fig. 17.2C).
n Focal atrial tachycardia: The tachycardia origi-
nates from a single focus in the atria or from a
venous connection contiguous to the atria such
as the pulmonary veins or vena cava.

Phase 4 rises slowly and fires Phase 4 is flat

automatically when it reaches and does not
threshold potential 1 reach threshold 1
2 2
Threshold
Potential 0 3 0
0 0 3

4 4 4
4 4
A B

Figure 17.1: Pacemaking and Non-pacemaking Cell. (A) Action potential

of pacemaking cells. Pacemaking cells exhibit slow diastolic depolarization during
phase 4 and discharge automatically when phase 4 reaches threshold potential.
(B) Action potential of non-pacemaking cells. In non-pacemaking cells, phase 4 is flat
and the action potential never reaches threshold. The numbers 0, 1, 2, 3, and 4
represent the different phases of the transmembrane action potential.

211
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212 Chapter 17
A B
Figure 17.2: Automatic Supraventricular Tachycardia (SVT). Automatic SVT can occur any-
where in the atria or atrioventricular junction. (A) Pathologic or inappropriate sinus tachycardia. (B) Focal
atrial tachycardia arising from a single focus in the atria. (C) Multifocal atria tachycardia showing multi-
ple foci in the atria. (D) Junctional tachycardia, which can be paroxysmal or nonparoxysmal.
n Multifocal atrial tachycardia: The tachycardia is
multifocal if several ectopic foci are present in
the atria.
AV junctional tachycardia: The tachycardia arises
from the AV junction, which includes the AV node
down to the bifurcation of the bundle of His (Fig.
17.2D). Junctional tachycardia can be paroxysmal or
nonparoxysmal.
n Nonparoxysmal junctional tachycardia: The
tachycardia arises from a focus in the AV junc-
tion and has a relatively slow rate of 70 to 120
beats per minute (bpm).
n Paroxysmal junctional tachycardia: The tachy-
cardia is paroxysmal because it starts abruptly
and terminates suddenly. The tachycardia has a
faster rate varying from 120 to 180 bpm.
Focal Atrial Tachycardia
Focal atrial tachycardia: Focal atrial tachycardia im-
plies that the tachycardia arises from a single location in
the atria. The atrial impulse spreads in a circumferential
manner regardless of the mechanism of the tachycardia.
Thus, the tachycardia may be due to enhanced auto-
maticity (automatic atrial tachycardia), intra-atrial
micro-reentry (intraatrial reentrant tachycardia), or
triggered automaticity (atrial tachycardia with 2:1 AV
block). The mechanisms underlying these tachycardias
cannot be differentiated from one another with a 12-
lead electrocardiogram (ECG). Because these tachycar-
dias all look similar, any tachycardia originating from a
single focus in the atria that spreads circumferentially is
focal atrial tachycardia (Figure 17.3).
The ECG findings of focal atrial tachycardia include
the following:
AV
Junction
C D
Presence of a regular narrow complex tachycardia
100 bpm.
Ectopic P waves, which are different from sinus P
waves, precede the QRS complexes usually with a PR
interval 0.12 seconds.
The P waves are uniform and the atrial rate varies to
as high as 250 bpm. The baseline between the P
waves is usually flat or isoelectric and not wavy or
undulating as in atrial flutter.
Second-degree or higher grades of AV block may oc-
cur because the tachycardia is not dependent on the
AV node.
The tachycardia terminates with a QRS complex in
contrast to reentrant SVT (atrioventricular nodal
reentrant tachycardia [AVNRT] and atrioventricu-
lar reentrant tachycardia [AVRT]), which usually
terminates with a retrograde P wave (Fig. 17.4).
Although nonsustained focal atrial tachycardia is fre-
quently seen during cardiac monitoring in the coro-
nary or intensive care units, sustained focal atrial
tachycardia is rare, occurring in 0.5% of sympto-
matic patients. The sustained form is slightly more
common in children than in adults but is also a rare
clinical entity. The tachycardia can be incessant (per-
sists more than 12 hours per day), which can result in
tachycardia-mediated cardiomyopathy.
Focal atrial discharges do not occur randomly. They
frequently cluster in certain areas in the atria such as
the mitral or tricuspid annulus, atrial appendages, os-
tium of the coronary sinus, and along the crista termi-
nalis. Spontaneous focal discharges from the pul-
monary veins are too small to be recorded in the
surface ECG, but have been recorded by intracardiac
techniques. These focal discharges can result in SVT
and have also been implicated as an important cause of
atrial fibrillation.
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Supraventricular Tachycardia due to Altered Automaticity 213

A.

During tachycardia Spontaneous conversion

to normal sinus rhythm
B.

Figure 17.3: Focal Atrial Tachycardia. (A) A 12-lead electrocardiogram showing focal
atrial tachycardia with a rate of 136 beats per minute. The P waves are uniform in configuration
and are upright in I, II, III, aVF, and V1. The tachycardia can be mistaken for sinus tachycardia.
(B) Lead II rhythm strip showing spontaneous conversion of the tachycardia to normal sinus
rhythm. Note that the P wave morphology is different during tachycardia and during normal
sinus rhythm. Note also that the tachycardia terminated with a QRS complex (block arrow) rather
than a retrograde P wave, suggesting that the SVT is due to focal atrial tachycardia.

Localizing the origin of the tachycardia: In focal
atrial tachycardia, the origin of the tachycardia may be
localized by the morphology of the P waves. The most
useful lead is V1 followed by lead aVL (see Fig. 17.5).
Right atrial vs left atrial origin:
n Right atrial origin: If the tachycardia is of right
atrial origin, the P waves are inverted in V1. If
biphasic in V1, the P waves are initially positive
(upright) and terminally negative (inverted). In
lead aVL, the P waves are upright or biphasic (Fig.
17.5A).
n Left atrial origin: If the tachycardia is left atrial in
origin, the P waves are upright in V1. If V1 is bipha-
sic, the P waves are initially negative (inverted)
and terminally positive (upright). In aVL, the P
waves are negative or isoelectric (flat) (Fig. 17.5B).

SVT Sinus Rhythm

Figure 17.4: Focal Atrial Tachycardia. The rhythm strip was recorded in lead II. The left
side of the rhythm strip shows focal atrial tachycardia with P waves between QRS complexes
(arrows). The tachycardia terminated spontaneously followed by a sinus P wave and back to back
ventricular complexes. Normal sinus rhythm followed as shown on the right side of the tracing.
Note that the tachycardia terminated with a ventricular complex (block arrow) rather than a P
wave. SVT terminating with a QRS complex is usually from focal atrial tachycardia. This type of
SVT may not respond to adenosine.
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214 Chapter 17

Figure 17.5: Focal Atrial Tachycardia. Right Atrial vs Left Atrial Origin of the SVT
The origin of the tachycardia can be identified
Lead V1 Lead aVL
as right atrial or left atrial based on the config-
uration of the P waves in leads V1 and aVL. If Right Atrial Focus
Sinus
the ectopic focus is in the right atrium (A), the Node
P waves are inverted in V1 or if biphasic are ini-
LA OR OR
tially upright and terminally negative. In lead
A. RA
aVL, the P waves are upright or biphasic. If the
ectopic focus is in the left atrium (B), the P AV Node
waves are positive in V1. If biphasic, the P
waves are initially inverted and terminally up-
right. In lead aVL, the P waves are isoelectric Lead V1 Lead aVL
(flat) or inverted. AV, atrioventricular; RA, right
Left Atrial Focus
atrium; LA, left atrium. Sinus
Node
LA OR OR
B. RA

AV Node

Localizing the tachycardia: ECG Findings of Focal Atrial Tachycardia

Superior versus inferior origin:
n Superior origin: If the tachycardia originates su-
periorly in either right or left atria, the P waves
are upright in II, III, and aVF. Superior origin of
the atrial tachycardia includes the atrial ap-
pendages and superior pulmonary veins (Fig.
17.6A). The tachycardia may be difficult to dif-
ferentiate from sinus tachycardia.
n Inferior origin: If the tachycardia originates in-
feriorly in either right or left atria, the P waves
are inverted in leads II, III, and aVF. Inferior ori-
gin of the atrial tachycardia includes the inferior
vena cava and coronary sinus orifice as well as
the inferior pulmonary veins (Fig. 17.6B).
Examples of focal atrial tachycardia are shown in
Figs. 17.7 to 17.10.
1. Presence of a regular narrow complex tachycardia 100 bpm.
2. The P waves are uniform in configuration but are different
in morphology when compared with P waves of normal
sinus origin.
3. The P waves precede the QRS complexes with a PR interval
shorter than the R-P interval. This finding, however, may be
reversed depending on the integrity of the AV node and pres-
ence of AV conduction abnormality. The PR interval generally
measures 0.12 seconds.
4. Second degree or higher grades of AV block may occur because
the tachycardia is not dependent on the AV node.
5. The baseline between 2 P waves is isoelectric unlike atrial flut-
ter where the baseline is wavy and undulating.
6. The tachycardia terminates with a QRS complex rather than a
P wave.

Figure 17.6: Focal Atrial Tachycardia. If the P waves Superior Lead II, III and aVF
are upright in II, III and aVF, the origin of the tachycardia is in
the superior right or left atria (A). If the P waves are inverted
A
in II, III, and aVF, the origin of the tachycardia is in the inferior Atria
right or left atria (B).
Lead II, III and aVF

Atria
B
Inferior
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Supraventricular Tachycardia due to Altered Automaticity
Mechanism
Focal atrial tachycardia is a type of SVT originating from a
single focus in the atria. The impulse spreads to the atria in a
circumferential manner. The mechanism of the tachycardia
may be due to intraatrial reentry, enhanced automaticity, or
triggered activity. These mechanisms are impossible to differ-
entiate using the 12-lead ECG. Focal atrial tachycardia do not
occur at random but originate more commonly in the right
atrium as well as veins that drain directly into the atria such as
the pulmonary veins, vena cava, and coronary sinus. They can
also originate from the atrial appendages, mitral or tricuspid
annulus, left side of the atrial septum, and crista terminalis.
The P waves are uniform in configuration because the tachy-
cardia originates from a single focus. The PR interval is usu-
ally 0.12 seconds in duration because the impulse has to
travel within the atria and across the AV node before reach-
ing the ventricles. The configuration of the P waves is differ-
ent from P waves of normal sinus rhythm and is helpful in
identifying the origin of the tachycardia.
When the tachycardia originates from the right atrium,
the P waves are inverted in V1. If biphasic, the P wave is
initially upright and terminally inverted. The P waves are
upright in lead aVL or it may be biphasic. Right atrial ori-
gin of the tachycardia includes the crista terminalis, tri-
cuspid annulus, ostium of the coronary sinus, and right
atrial appendage.
When the tachycardia originates from the left atrium, the P
waves are upright in V1. If biphasic, the P wave is initially
inverted and terminally upright. The P waves are isoelectric
(flat) or negative (inverted) in lead aVL. Left atrial tachy-
cardia includes the pulmonary veins, mitral annulus, left
side of the atrial septum, and left atrial appendage.
When the tachycardia originates inferiorly from either
atria, the P waves are inverted in leads II, III, and aVF.
When the tachycardia originates superiorly from either
atria, the P waves are upright in leads II, III, and aVF.
The PR as well as the R-R interval may vary during the tachy-
cardia, especially if the SVT is due to enhanced automaticity.
This is in contrast to reentrant SVT, where these intervals are
usually fixed and regular because the reentrant SVT follows a
fixed pathway.
Clinical Implications
Nonsustained or short episodes of focal atrial tachycardia oc-
cur very frequently during monitoring. Sustained focal atrial
tachycardia however is uncommon, occurring in 0.5% of
symptomatic patients.
Focal atrial tachycardia can be incessant (persists for more
than 12 hours per day). This can result in tachycardia-
mediated cardiomyopathy, which is more common in infants
and young children because they are unable to communicate
their symptoms when having the tachycardia. Although
215
tachycardia-mediated cardiomyopathy from focal atrial
tachycardia is not common, it is one of the few causes of di-
lated cardiomyopathies that can be reversed if the arrhyth-
mia is identified and successfully treated.
If the tachycardia originates from the right atrium close to the
sinus node, or in the right superior pulmonary vein, the tachy-
cardia may be mistaken for sinus tachycardia. Atrial tachycar-
dia with 2:1 AV block can be mistaken for atrial flutter with 2:1
AV block. In atrial tachycardia with block, the baseline be-
tween 2 P waves is isoelectric, unlike atrial flutter where the
baseline between 2 flutter waves is wavy and undulating. The
treatment for these different arrhythmias is not the same.
Focal atrial tachycardia can also be mistaken for atypical
AVRT, atypical AVNRT, and junctional tachycardia. All these
arrhythmias have P waves preceding the QRS complex with a
shorter PR than R-P interval. In general, atypical AVRT and
atypical AVNRT may be terminated with vagal maneuvers or
with AV nodal blockers. When AVNRT or AVRT terminates,
the last part of the tachycardia is a retrograde P wave. In fo-
cal atrial tachycardia, the SVT terminates with a QRS com-
plex. This type of tachycardia should be recognized because
this may not respond to adenosine.
The size of the P wave may also be useful in identifying a ret-
rograde P wave originating from the AV node. Because the
AV node is in the lower mid-atria, the retrograde P waves
may be narrow in AVNRT and in AV junctional tachycardia
since both atria are activated simultaneously, whereas the P
waves from focal atrial tachycardia or AVRT are broader.
Focal atrial tachycardia may be due to acute myocarditis,
chronic cardiomyopathy, or a local pathology in the atria
such as an atrial tumor. It can also occur spontaneously in
muscle sleeves of veins directly draining into the atria such as
the pulmonary veins, vena cava, and coronary sinus. These
cells may possess automatic properties similar to that of the
sinus node and become the dominant pacemakers of the
heart when their firing rate is enhanced. Focal atrial tachy-
cardia can be due to pharmacologic agents such as dobuta-
mine and other catecholamines, theophylline, caffeine, and
nicotine. When focal atrial tachycardia is due to digitalis tox-
icity, the tachycardia is usually associated with 2:1 AV block.
The atrial impulse is conducted to the ventricles through the
normal AV conduction system. AV block can occur because
the tachycardia is not dependent on the AV node. Vagal ma-
neuvers and AV nodal blockers (adenosine, beta blocker, cal-
cium channel blockers, and digitalis) can slow down the ven-
tricular rate by causing AV block, but may not terminate the
arrhythmia. However, if the mechanism of the SVT is due to
micro-reentry or triggered activity, the tachycardia may be
responsive to adenosine or verapamil.
Acute Treatment
If the tachycardia is due to digitalis toxicity, digitalis
should be discontinued. Digitalis toxicity is enhanced by
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216 Chapter 17

hypokalemia, hypomagnesemia, and hypercalcemia. These
electrolyte abnormalities should be corrected. Potassium
supplements are usually given to minimize the effects of
digitalis toxicity. The use of digoxin binding agents should
be considered if the arrhythmia is persistent and is poorly
tolerated.
Tachycardia is also precipitated by metabolic and blood gas
disorders or use of pharmacologic agents such as theo-
phylline, albuterol, or catecholamines. These metabolic and
respiratory abnormalities should be corrected and the of-
fending agents should be discontinued.
Because focal atrial tachycardia is a regular narrow complex
tachycardia, the tachycardia is difficult to distinguish from
atypical AVNRT and atypical AVRT. Thus, the acute treat-
ment for the tachycardia is similar to any regular narrow
complex SVT. These include vagal maneuvers, AV nodal
blockers such as adenosine, beta blocker, calcium channel
blockers, and digitalis (if digitalis is not the cause of the
tachycardia). A significant number of focal atrial tachycardia
(atrial tachycardia due to microreentry or triggered activity)
may respond to adenosine or verapamil. Thus, adenosine re-
mains the drug of choice for any regular narrow complex
tachycardia and should be tried before other agents are con-
sidered. If the tachycardia is not responsive to adenosine or
AV block occurs without converting the SVT to normal sinus
rhythm, longer acting AV nodal agents such as diltiazem, ve-
rapamil, or beta blockers can be given to slow down the ven-
tricular rate by causing AV block.
Focal atrial tachycardia from enhanced automaticity gener-
ally will not respond to adenosine. Class IA (procainamide),
Class IC (flecainide and propafenone), or Class III (sotalol,
amiodarone) antiarrhythmic agents should be considered
if adenosine and other AV nodal blocking agents are not
effective.
Electrical cardioversion is not effective when the mechanism
of the tachycardia is due to enhanced automaticity but may
be effective if the tachycardia is due to intra-atrial reentry or
triggered activity. Unless patient is in circulatory shock, elec-
trical cardioversion is contraindicated when the tachycardia
is known to be due to digitalis toxicity (atrial tachycardia
with 2:1 AV block with history of digitalis intake) or the
tachycardia is due to metabolic or electrolyte abnormalities.
When the tachycardia is intractable to medical therapy, elec-
trical ablation (or if not feasible, surgical excision) of the ar-
rhythmogenic focus should be considered.
Prognosis
In infants and young children, in whom the tachycardia is
more difficult to detect, the mortality is high because a tachy-
cardia-mediated cardiomyopathy may occur. This type of
cardiomyopathy is reversible if the tachycardia is recognized
as the cause of the cardiomyopathy.
Focal atrial tachycardia is usually associated with structural
cardiac diseases. The prognosis will depend on the etiology
of the cardiac abnormality. The overall prognosis of focal
atrial tachycardia from digitalis excess and metabolic, respi-
ratory, or electrolyte abnormalities will depend on the un-
derlying condition. In the absence of structural cardiac dis-
ease, the overall prognosis is generally good.

Figure 17.7: Focal Atrial Tachycardia. The electrocardiogram is from a patient with acute exacerbation of
asthma.The P waves are inverted in aVL and are upright in leads II, III, and aVF suggesting a superior left atrial origin
of the impulse. Electrical alternans is seen in leads II and in all precordial leads (arrows). Although electrical alternans
is frequently associated with AVRT, it is also seen in other types of supraventricular tachycardia as shown here. AVRT,
atrioventricular reentrant tachycardia.
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Supraventricular Tachycardia due to Altered Automaticity 217

Figure 17.8: Focal Atrial Tachycardia. The P waves are inverted in leads II, III, and aVF and upright in V1. The
PR interval is 0.12 seconds and the R-P interval is longer than the PR interval. This type of SVT is usually due to fo-
cal atrial tachycardia originating from the inferior wall of the left atrium. The above SVT, however, is difficult to differ-
entiate from atypical AVNRT, atypical AVRT, or junctional tachycardia. Because the P waves are broad, the SVT is more
likely the result of focal atrial tachycardia or AVRT rather than AVNRT or junctional tachycardia. SVT, supraventricular
tachycardia; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia.

Focal Atrial Tachycardia

Figure 17.9: Focal Atrial Tachycardia with Second-Degree

Atrioventricular (AV) Block. The P waves precede the QRS complexes
and are inverted in leads II, III, and aVF, negative in aVL, and upright in V1.
There is gradual prolongation of the PR interval until a ventricular complex is
dropped (arrows). Because second-degree AV block is present, AVRT is not
possible and AVNRT is highly unlikely. AVNRT, atrioventricular nodal reentrant
tachycardia; AVRT, atrioventricular reentrant tachycardia.
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218 Chapter 17

Figure 17.10: Focal Atrial Tachycardia with Second-Degree Atrioventricular (AV) Block. A 12-lead
electrocardiogram showing focal atrial tachycardia with second-degree AV Wenckebach. The P waves precede the
QRS complexes with a rate of 150 beats per minute. The mechanism of the focal atrial tachycardia was thought to
be IART because the patient had previous atrial septal defect repair, which is a possible focus of reentry. The patient
was successfully cardioverted electrically to normal sinus rhythm. Focal atrial tachycardia from enhanced automatic-
ity generally does not respond to electrical cardioversion. The presence of AV block excludes AVRT and upright P
waves in II, III, and aVF makes AVNRT unlikely. AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventric-
ular reentrant tachycardia; IART, intraatrial reentrant tachycardia. Arrows point to the nonconducted P waves.

Typical examples of MAT are shown in Figures 17.12 to

Multifocal Atrial Tachycardia 17.14.

Multifocal atrial tachycardia (MAT): MAT is charac- ECG Findings of MAT

terized by the presence of atrial complexes originating
1. At least three consecutive P waves with different morphologies
from different foci in the atria. The P waves are irregu-
with a rate 100 bpm should be present.
lar with varying sizes and shapes and varying PR and
R-R intervals (Figs. 17.1117.14). Because the R-R 2. The PR as well as the R-R interval is variable with isoelectric
baseline between P waves.
intervals are irregular, the arrhythmia can be mistaken
for atrial fibrillation.
Mechanism
The diagnosis of MAT is based on the presence of three
or more consecutive P waves of different morphologies MAT is most probably due to enhanced automaticity. Multi-
with an isoelectric baseline between P waves with a rate ple independent automatic foci are present in the atria, re-
100 bpm. sulting in varying configurations of the P wave.

Figure 17.11: Multifocal Atrial Tachycardia

Atria
(MAT). Diagrammatic representation of MAT show-
ing at least three consecutive P waves of different
sizes and shapes with a rate 100 beats per minute.

Multifocal atrial tachycardia (MAT).

Ventricle
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Supraventricular Tachycardia due to Altered Automaticity 219

Figure 17.12: Multifocal Atrial Tachycardia (MAT). The electrocardiogram shows MAT. For MAT to be pres-
ent, three consecutive P waves of varying morphologies should be present with a rate 100 beats per minute. The
rate is irregular, the PR intervals are variable, and the baseline between two P waves is isoelectric.

Clinical Implications
MAT is also called chaotic atrial tachycardia. When the rate is
100 bpm, the arrhythmia is often called chaotic atrial rhythm
or multifocal atrial rhythm. Because of the irregular heart
rate, the tachycardia is often mistaken for atrial fibrillation.
MAT is commonly seen in elderly patients with acute exacer-
bations of chronic obstructive pulmonary disease (COPD)
as well as those with electrolyte or metabolic abnormalities
and pulmonary infection. Most of these patients with acute
exacerbations of COPD are on theophylline or beta agonists.
These medications are implicated as the cause of the MAT.
Acute Treatment
Treatment of the tachycardia is directed toward the underly-
ing cause, which is usually COPD. If the patient is on theo-
phylline or beta agonist, the drug should be discontinued.

Figure 17.13: Multifocal Atrial Tachycardia (MAT). In MAT, the QRS complexes are preceded by P waves of
varying sizes and shapes. At least three consecutive P waves with varying morphologies are present with a rate over
100 beats per minute (arrows).
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220 Chapter 17
Figure 17.14: Multifocal Atrial Tachycardia. Note the presence of P waves of varying morphologies pre-
ceding each QRS complex (arrows) in the long lead rhythm strip at the bottom of the tracing. The baseline
between P waves remains isoelectric.
Any electrolyte, blood gas, or metabolic abnormality should
be corrected. Any associated cardiac disease or pulmonary
infection should be treated.
MAT should be differentiated from atrial fibrillation. Pa-
tients with atrial fibrillation need to be anticoagulated,
whereas patients with MAT do not need anticoagulation.
The rate of the tachycardia is usually not rapid and usually
does not exceed 130 bpm. However, because MAT occurs more
frequently in elderly individuals with COPD, the rate may not
be tolerable especially when there is heart failure, ischemic
heart disease, or respiratory insufficiency. Pharmacologic ther-
apy may be necessary to control the rate of the tachycardia.
Nondihydropyridine calcium channel blockers may be used to
control the ventricular rate and diminish the number of ec-
topic atrial impulses. Diltiazem (20 mg IV) or verapamil (5 to
10 mg IV) may be given intravenously. Diltiazem may be
continued as an IV infusion drip at 5 to 15 mg per hour af-
ter the rate has been controlled with the initial bolus. Vera-
pamil should not be given if there is left ventricular dys-
function (ejection fraction 40%) or there is heart failure.
Although beta blockers are also effective, these drugs are
usually contraindicated because MAT is frequently seen in
the setting of bronchospastic pulmonary disease. In pa-
tients without reactive airway disease, beta blockers are ef-
fective agents.
Although antiarrhythmic agents are usually not indicated
for MAT, amiodarone may be tried for rate control and
for suppression of ectopic atrial impulses if the arrhyth-
mia has not improved with the above agents. Magne-
sium given intravenously has also been used with varying
success when other agents have failed even in the absence
of hypomagnesemia.
Digitalis is not effective and has a narrow margin of safety
in patients with chronic pulmonary disease and should
not be given.
MAT frequently deteriorates to atrial fibrillation. The rate
in atrial fibrillation may be easier to control than the rate
in MAT; however, anticoagulation may be necessary.
Electrical cardioversion has no place in the therapy of MAT.
MAT is an example of SVT from enhanced automaticity and
electrical cardioversion will not be effective.
Prognosis
The arrhythmia is usually well tolerated and prognosis de-
pends on the underlying medical condition.
Junctional Tachycardia
Junctional tachycardia: AV junctional tachycardia is
due to repetitive impulses originating from the AV
node or bundle of His. The impulse follows the normal
AV conduction system resulting in narrow QRS com-
plexes. There are two types of junctional tachycardia:
Nonparoxysmal junctional tachycardia: The SVT
has a slower rate of 70 to 120 bpm. Despite the very
slow rate of 100 bpm, the arrhythmia is considered
a tachycardia since the intrinsic rate of the AV junc-
tion is exceeded, which is usually 40 to 60 bpm (Fig.
17.15). AV junctional rhythm with a rate 100 bpm
is more appropriately called accelerated junctional
rhythm rather than junctional tachycardia. The
tachycardia is nonparoxysmal with a slow onset and
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Supraventricular Tachycardia due to Altered Automaticity 221

Figure 17.15: Nonparoxysmal Junctional Tachycardia. No P waves are noted in the entire 12-lead electro-
cardiogram. Although the ventricular rate is 100 beats per minute, the arrhythmia is accepted as junctional tachy-
cardia since the rate exceeds the intrinsic rate of the atrioventricular junction, which is 60 beats per minute.

termination. This type of tachycardia may be due to Lead II

enhanced automaticity or triggered activity. Atria

Paroxysmal or focal junctional tachycardia:

This type of tachycardia is rare. The tachycardia is A
also called junctional ectopic tachycardia or auto- Pseudo q waves PR interval <0.12 second
matic junctional tachycardia. The American College
of Cardiology/American Heart Association Task
Force on Practice Guidelines/European Society of Atria
Cardiology guidelines on SVT refer to this tachycar-
dia as focal junctional tachycardia. The tachycardia B
varies from 110 to 250 bpm and is often paroxysmal No P waves
with sudden onset and abrupt termination. The
mechanism of the tachycardia is due to enhanced
automaticity or triggered activity.
Atria
ECG findings: The ECG of AV junctional tachycardia
overlaps those of other SVT. Because the tachycardia is
C
not dependent on the atria or ventricles, the relation-
ship between the P wave and the QRS complex is vari- R-P interval 0.20 second

able. The retrograde P waves are narrow and may occur

before or after the QRS complex. It may also be syn-
Atria
chronous with the QRS complex. When this occurs, the #1: Normal Sinus Rhythm #2: Atrial Fibrillation
P waves are not visible. The diagrams in Fig. 17.16
summarize the ECG findings of junctional tachycardia. D

Complete AV Dissociation

Nonparoxysmal Junctional
Tachycardia
When the retrograde P wave precedes the QRS com-
plex, the PR interval is usually 0.12 seconds. The
width of the retrograde P wave is usually thinner than
a normal sinus P wave, because the impulse originates
from the AV node. Thus, both atria are activated
Figure 17.16: Junctional Tachycardia. (A) Atrial
activation occurs earlier than ventricular activation (P wave is in
front of the QRS complex). (B) Atrial activation is synchronous
with ventricular activation (no P waves are present). (C) Ventric-
ular activation occurs earlier than atrial activation (P waves oc-
cur after the QRS complex). (D) Complete atrioventricular disso-
ciation during normal sinus rhythm (#1) and during atrial
fibrillation (#2).
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222 Chapter 17

Figure 17.17: Nonparoxysmal Junctional Tachycardia. Lead II rhythm strip showing accelerated junctional
rhythm at 87 beats per minute. Retrograde P waves are inscribed just before the QRS complexes (arrows), which can
be mistaken for Q waves (pseudo-Q waves). Note that the P waves are narrow measuring less than 0.05 seconds.

Figure 17.18: Nonparoxysmal Junctional Tachycardia. Lead II rhythm strip again showing accelerated
junctional rhythm at 73 beats per minute. Note that the retrograde P waves are inscribed after the QRS complexes
and are narrow (arrows). Because the P waves occur during ventricular systole, this can result in cannon A waves in
the jugular neck veins.

Figure 17.19: Nonparoxysmal Junctional Tachycardia. The initial half of the tracing shows nonparoxysmal
junctional tachycardia of 106 beats per minute. There is isorhythmic atrioventricular dissociation (arrows) until the
sinus P waves capture the QRS complexes at a slightly higher rate of 110 beats per minute.

Figure 17.20: Accelerated Junctional Rhythm with Complete Atrioventricular Dissociation. The
atrial and ventricular rates are almost similar at 80 beats per minute. The sinus P waves however are completely dis-
sociated from the QRS complexes. Arrows point to the P waves.
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Supraventricular Tachycardia due to Altered Automaticity 223

A. During tachycardia

B: Upon conversion to normal sinus rhythm

Figure 17.21: Paroxysmal Junctional Tachycardia. (A) Twelve-lead electrocardiogram (ECG) of a 6-year-old
boy with paroxysmal tachycardia with a rate of 206 beats per minute. There are no P waves during tachycardia and
is consistent with paroxysmal junctional tachycardia. (B) A 12-lead ECG on conversion to normal sinus rhythm.

simultaneously. When it follows the QRS complex, the
R-P interval is usually 0.20 seconds.
The rate of the tachycardia can be enhanced by sympa-
thetic or parasympathetic manipulation. Atropine,
dobutamine and other adrenergic agents can increase
the rate of the tachycardia. Examples of nonparoxys-
mal junctional tachycardia are shown in Figures 17.17
through 17.20.
Paroxysmal Junctional Tachycardia
Paroxysmal or focal junctional tachycardia is rare. The
SVT is more commonly seen in children than in
adults. Shown is a 12-lead ECG of a 6-year-old boy
with paroxysmal tachycardia from focal junctional
tachycardia. The tachycardia has no P waves making it
difficult to differentiate from AV nodal reentrant
tachycardia (Fig. 17.21).
ECG Findings of Junctional Tachycardia
The ECG findings of nonparoxysmal and paroxysmal or fo-
cal junctional tachycardia are similar except for the differ-
ence in rate, onset, and termination of the tachycardia.
1. The QRS complexes are narrow unless there is preexistent
bundle branch block or the impulse is conducted with aber-
ration.
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224 Chapter 17
2. The QRS complexes are regular. In focal junctional tachy-
cardia, the ventricular rate is 110 to 250 bpm. In nonparox-
ysmal junctional tachycardia, the ventricular rate is slower
and varies from 70 to 130 bpm.
3. The P waves may occur synchronously with the QRS com-
plex and may not be visible.
4. When P waves are present, they are retrograde and are in-
verted in leads II, III, and aVF. The retrograde P waves may
occur before or after the QRS complexes. When the retro-
grade P waves occur before the QRS complexes, the PR in-
terval is short and is usually 0.12 seconds. When the ret-
rograde P waves follow the QRS complexes, the R-P interval
is usually 0.20 seconds.
5. Complete AV dissociation may occur since the tachycardia
does not need the atria (or the ventricles) for its participa-
tion. The sinus node captures the atria; however, the ventri-
cles are separately controlled by the junctional tachycardia
resulting in complete AV dissociation.
6. A junctional tachycardia can also occur in the presence of
atrial fibrillation resulting in regularization of the R-R interval
since the ventricles are completely dissociated from the atria.
Mechanism
The AV junction includes the whole AV node down to the bi-
furcation of the bundle of His. The AV node consists of three
parts with distinct electrophysiologic properties. The superior
portion of the AV node is the atrionodal or AN region, which
lies directly adjacent to the atria. The middle portion of the AV
node is the main body or nodal (N) region and the distal part
that is directly contiguous to the bundle of His is the nodo-His
or NH region. The AV junction, excluding the middle portion
of the AV node, contains cells with automatic properties that
may compete with the sinus node as the pacemaker of the heart.
Although cells in the AV junction have automatic properties,
the intrinsic rate of these cells is slower than that of the sinus
node. These cells therefore are normally depolarized by the
spread of the faster sinus impulse and serve as latent or backup
pacemakers. When the firing rate of the cells in the AV junction
is enhanced and becomes faster than the rate of the sinus node,
junctional rhythm may become the dominant rhythm.
The junctional rhythm may control both atria and ventricles
simultaneously. The impulse is conducted anterogradely to
the ventricles through the normal conduction system result-
ing in QRS complexes that are narrow, similar to the QRS
complexes of normal sinus rhythm. The P waves are retro-
grade and are inverted in leads II, III, and aVF because the
atrial impulse travels from below upward in the atria. The
retrograde P waves are narrower (thinner) than the normal
sinus P waves because the atria are activated simultaneously
when the rhythm starts from the AV junction.
The retrograde P waves may occur in front of the QRS
complexes if retrograde conduction of the junctional im-
pulse to the atria is faster than anterograde conduction to
the ventricles.
The retrograde P waves may follow the QRS complex if
anterograde conduction of the impulse to the ventricles is
faster than retrograde conduction to the atria.
The P waves may not be visible if conduction of the im-
pulse to the atria and ventricles are synchronous resulting
in simultaneous activation of both chambers. When this
occurs, the smaller P wave will be embedded within the
larger QRS complexes and will not be visible.
The junctional rhythm may also control the ventricles but
not the atria, if retrograde conduction of the impulse is
blocked at the AV node. When this occurs, the sinus node
may retain control of the atria resulting in complete or in-
complete AV dissociation. If there is atrial fibrillation, the
ventricles are controlled independently by a junctional
impulse causing the R-R intervals to become regular. This
is usually the case when there is digitalis toxicity.
Nonparoxysmal junctional tachycardia may be due to en-
hanced automaticity involving cells within the AV junction or
it may be due to triggered activity. Triggered activity as a mech-
anism for tachycardia usually occurs when conditions are ab-
normal, such as when there is digitalis toxicity, increased intra-
cellular calcium, or marked adrenergic activity. Digitalis
prevents the exchange of sodium and potassium during repo-
larization by inhibiting the enzyme Na/K ATPase. The build
up of Na inside the cell causes the Na/Ca exchange mech-
anism to be activated resulting in accumulation of Ca inside
the cell. The increased Ca inside the cell is the mechanism
by which digitalis exerts its positive inotropic effect. When
there is digitalis toxicity, the less negative membrane potential
due to calcium overload may trigger afterdepolarizations to
occur during phase 4 of the action potential. These afterdepo-
larizations may reach threshold potential resulting in a series
of action potentials that may become sustained. Nonparoxys-
mal junctional tachycardia and atrial tachycardia with 2:1
block are arrhythmias that are usually due to digitalis toxicity
(see SVT due to Triggered Activity in this chapter).
Clinical Implications
Nonparoxysmal Junctional Tachycardia
Most junctional tachycardia seen in the adult is nonparoxysmal.
The tachycardia is relatively common and the diagnosis can be
made fairly easily. It has a rate of 70 to 120 bpm. Although the
rate of the tachycardia could be 100 bpm, the arrhythmia is
traditionally accepted as tachycardia because it exceeds the in-
trinsic rate of the AV junction, which is 40 to 60 bpm. Junc-
tional impulses with rates 100 bpm are preferably called ac-
celerated junctional rhythm rather than junctional tachycardia.
The tachycardia is nonparoxysmal because of its gradual on-
set and termination. The tachycardia is usually self-limiting,
often lasting for a few hours to a few days even without ther-
apy. Although the arrhythmia is benign and may not be asso-
ciated with any hemodynamic abnormalities, nonparoxysmal
junctional tachycardia may be a marker of a serious under-
lying cardiac condition because the tachycardia usually occurs
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Supraventricular Tachycardia due to Altered Automaticity
in the setting of acute inferior myocardial infarction, my-
ocarditis, congestive heart failure, hypokalemia, digitalis toxi-
city, and use of pharmacologic agents such as dobutamine
and other sympathomimetic agents. The arrhythmia can also
occur after cardiac surgery. It may be a manifestation of sick
sinus syndrome. It may also occur in normal individuals.
The rate of nonparoxysmal junctional tachycardia is relatively
slow; thus, the arrhythmia is usually tolerable and may not
cause any symptom. However, because the QRS complexes are
not preceded by P waves, the tachycardia may result in hemo-
dynamic deterioration because of loss of atrial contribution to
left ventricular filling especially in patients with left ventricular
dysfunction. This can result in low cardiac output and hy-
potension. When retrograde P waves follow the QRS complex,
atrial contraction occurs during ventricular systole, when the
AV valves are closed, resulting in cannon A waves in the neck
and pulmonary veins. This can cause hypotension and low
cardiac output mimicking the symptoms of pacemaker syn-
drome (see Chapter 26, The ECG of Cardiac Pacemakers).
Nonparoxysmal junctional tachycardia is seldom incessant
(the tachycardia seldom persists 12 hours a day). When this
occurs, a tachycardia-mediated cardiomyopathy can occur.
This complication is more frequently seen in focal junctional
tachycardia, which has a faster rate and is more common in
infants and children, most of whom are unable to complain
of symptoms related to the arrhythmia.
Focal Junctional or Paroxysmal
Junctional Tachycardia
Focal junctional tachycardia is rare in adults. It is also rare, but
is more common in children. Paroxysmal junctional tachycar-
dia has a rate of 110 to 250 bpm. The tachycardia is paroxysmal
because of its sudden onset and abrupt termination. The
tachycardia is also called junctional ectopic tachycardia or au-
tomatic junctional tachycardia. The tachycardia may be associ-
ated with congenital heart disease such as ventricular or atrial
septal defects, although they are also seen in structurally nor-
mal hearts. They can also occur during the immediate post-
operative period. When the tachycardia is incessant, meaning
the tachycardia occurs more than 12 hours per day, it may cause
a tachycardia-mediated cardiomyopathy especially in children.
Acute Treatment
Focal Junctional Tachycardia
Nonparoxysmal Junctional Tachycardia
Nonparoxysmal junctional tachycardia has a relatively slow
rate, is very well tolerated, and often self-limiting and gener-
ally does not need any drug therapy. It may be related to an
underlying abnormality, which should be recognized and
corrected. This includes electrolyte and metabolic abnormal-
ities such as hypokalemia, blood gas disturbances, chronic
obstructive pulmonary disease, myocardial ischemia, or in-
flammatory disorders involving the myocardium. It can also
be triggered by digitalis toxicity and use of dobutamine and
other sympathomimetic agents.
225
The presence of nonparoxysmal junctional tachycardia or ac-
celerated junctional rhythm with a rate of 100 bpm may be
a sign of underlying sinus node disease. When sinus node
dysfunction is suspected, the junctional rhythm should not
be suppressed.
Nonparoxysmal junctional tachycardia is frequently due to
digitalis toxicity. Digitalis should be discontinued if the drug
is the cause of the tachycardia. If digitalis is continued inap-
propriately, it may result in more serious, even fatal, arrhyth-
mias. The arrhythmia can be monitored without additional
therapy if the rate of the tachycardia is 100 bpm and the
patient is hemodynamically stable. Any electrolyte or meta-
bolic abnormality should be corrected. If the tachycardia is
rapid or there is hypokalemia, potassium supplements
should be given. Potassium should also be given if the serum
level is 4 mEq/L, especially in postoperative patients. The
rate of the tachycardia can be slowed with phenytoin 5 to 10 mg/
kg IV given as a 250-mg bolus diluted with saline and in-
jected IV slowly over 10 minutes, followed by 100 mg IV
every 5 minutes as needed to a maximum dose of 1 g. Pheny-
toin is effective only if the tachycardia is digitalis induced.
Side effects of hypotension, profound bradycardia, or respi-
ratory depression can occur especially if the phenytoin is
rapidly administered. Beta blockers given IV have also been
used to control the ventricular rate (see Appendix, Com-
monly Used Injectable Pharmacologic Agents, specifically
sections on intravenous dosing with metoprolol, atenolol, es-
molol, or propranolol). Treatment with digoxin-immune
Fab fragments should be considered if the arrhythmia is life-
threatening or the patient is hemodynamically unstable and
digitalis toxicity is the cause of the tachycardia. It should also
be given if the digoxin level exceeds 10 ng/mL.
The pharmacologic treatment of nonparoxysmal junctional
tachycardia not due to digitalis toxicity is similar to that of
focal junctional tachycardia.
In patients with accelerated junctional rhythm (nonparoxys-
mal junctional tachycardia) with retrograde P waves occur-
ring during ventricular systole associated with symptoms of
hypoperfusion and low cardiac output mimicking the pace-
maker syndrome, temporary atrial or AV sequential pacing is
usually effective.
If the rate of the tachycardia is unusually rapid, such as the case
with focal junctional tachycardia, the tachycardia should be
treated like any regular narrow complex tachycardia. Although
focal junctional tachycardia is rare, the ECG findings mimic
those of AVNRT, AVRT, and focal atrial tachycardia, which are
more common and are more responsive to adenosine. Thus,
adenosine should be tried initially and if not effective, beta
blockers or nondihydropyridine calcium channel blockers
should be tried (see Treatment of AVNRT in this chapter).
If AV nodal blockers are not effective, type IC (flecainide or
propafenone) and type III (amiodarone or sotalol) agents
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226 Chapter 17
may be tried to suppress the ectopic focus. The choice of
antiarrhythmic agent should be based on the presence or ab-
sence of left ventricular dysfunction. When left ventricular
dysfunction is present, amiodarone is the preferred agent.
In patients who do not respond to medications or in pa-
tients in whom the tachycardia continues to become recur-
rent or incessant, catheter ablation may be considered. Ab-
lative procedures may be associated with some risk of AV block
because the foci involves the AV node and bundle of His.
Prognosis
Nonparoxysmal junctional tachycardia is usually associated
with structural cardiac disease or digitalis excess but the ar-
rhythmia itself is self limiting. Focal junctional tachycardia
may also occur in structurally normal hearts and is more
common in pediatric patients and young adults. If the tachy-
cardia becomes incessant, it may result in tachycardia-
mediated cardiomyopathy.
The overall prognosis depends on the underlying cardiac dis-
ease associated with the tachycardia.
SVT from Triggered Activity
Triggered activity: Another possible mechanism of
SVT is triggered activity. Triggered activity is due to the
presence of afterdepolarizations. These are additional
depolarizations that are triggered by the previous ac-
tion potential. Afterdepolarizations may be single or
repetitive and may not always reach threshold poten-
tial. However, when these afterdepolarizations reach
threshold potential, repetitive firing may result in sus-
tained arrhythmia. This is unlike enhanced automatic-
ity, which is not dependent on the previous impulse
but is caused by automatic firing of a cell because of the
presence of phase 4 diastolic depolarization. Afterde-
polarizations occur when conditions are abnormal,
such as when there is digitalis toxicity or when there is
excess calcium or catecholamines.
A. Early Afterdepolarizations B. Late Afterdepolarizations
1
1
2 2
0 mv
0 3 0 3
Threshold Potential
4 4 4
Figure 17.22: Triggered Activity. (A) Triggered activity from
early afterdepolarizations (phase 2 or 3 of the action potential).
(B) Triggered automaticity from late afterdepolarizations (phase
4 of the action potential). The dotted line represents threshold
potential and 0, 1, 2, 3, and 4 represent the different phases of the
action potential. The arrows point to afterdepolarizations.
Triggered automaticity may be due to early or late
afterdepolarizations.
Early afterdepolarizations: These are afterdepo-
larizations that occur during phase 2 or phase 3 of
the action potential (Fig. 17.22A).
Late afterdepolarizations: These are afterdepo-
larizations that occur during phase 4 of the action
potential (Fig. 17.22B).
The role of triggered activity as a cause of SVT is un-
certain except in atrial tachycardia with 2:1 AV block
and in nonparoxysmal junctional tachycardia. Both ar-
rhythmias are frequently associated with digitalis toxi-
city (Figs 17.23 to 17.25).
Atrial Tachycardia with 2:1 AV Block
Atrial tachycardia with 2:1 AV block: Atrial tachy-
cardia with 2:1 AV block is an arrhythmia resulting
from triggered activity. This tachycardia is almost al-
ways from digitalis toxicity. Digitalis excites atrial and
ventricular myocytes, which may result in atrial and
ventricular tachycardia. Digitalis also blocks the AV
node; thus, the combination of atrial tachycardia with
AV block usually in a 2:1 ratio, is most commonly an
arrhythmia related to digitalis toxicity (Fig. 17.24). The
tachycardia arises from a single focus in the atria close
to the sinus node, causing the P wave to be upright in
leads II, III, and aVF, resembling sinus tachycardia
(Figs. 17.25).
Atrial tachycardia with varying degrees of AV block
may occur in patients who are not on digitalis. In these
patients, the mechanism for the tachycardia may be
due to enhanced automaticity rather than triggered ac-
tivity.
Fig. 27.26 summarizes the different ECG patterns of
narrow complex SVT and Fig. 27.27 is an algorithm
how to diagnose narrow complex tachycardias.
A B
Figure 17.23: Supraventricular Tachycardia (SVT) from
Triggered Activity. (A) Atrial tachycardia with 2:1 atrioven-
tricular block is an example of SVT due to triggered activity.The
ectopic focus (arrow) usually originates from the right atrium
close to the sinus node (arrow). (B) Nonparoxysmal junctional
tachycardia arising from the AV junction (arrow).
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Supraventricular Tachycardia due to Altered Automaticity 227

Lead II

Figure 17.24: Atrial Tachycardia with 2:1 Atrioventricular (AV) Block. The P waves (arrows) are upright
in lead II with a rate of 230 beats per minute. Atrial tachycardia with 2:1 AV block is usually from digitalis toxicity. The
configuration of the ST segment is typical of digitalis effect.

the atria (AVNRT or AVRT) is excluded. The most

Approach to a Patient with Narrow
Complex Tachycardia
When a narrow complex tachycardia with a QRS du-
ration of 0.12 seconds is present, the ECG should
first be inspected for gross irregularity of the R-R
intervals.
Grossly irregular R-R intervals (Fig. 17.28):
Multifocal atrial tachycardia: Distinct P waves of
different configurations are present preceding each
QRS complex.
Atrial fibrillation: The baseline shows fibrillatory
waves. No definite P waves or flutter waves are
present.
Atrial flutter: Flutter waves are present with a saw
tooth or undulating baseline.
Regular R-R intervals with no visible P waves
(Fig. 17.29):
AVNRT
Junctional tachycardia (paroxysmal or nonparo-
xysmal)
Narrow Complex Tachycardia with
Regular R-R Intervals
Regular R-R intervals with upright P waves in
front of the QRS complexes (Fig. 17.30): If the P
waves are upright in lead II, retrograde activation of
likely possibilities are:
Sinus tachycardia
Focal atrial tachycardia
Sinoatrial reentrant tachycardia
Regular R-R intervals with retrograde P waves in
front of the QRS complexes (Fig. 17.31): The pres-
ence of retrograde P waves in front of the QRS com-
plexes excludes sinus tachycardia and SART and favors:
Focal atrial tachycardia
Junctional tachycardia (paroxysmal or nonparo-
xysmal)
Atypical AVNRT
Atypical AVRT
Retrograde P waves between QRS complexes (Fig.
17.32): Retrograde P waves between QRS complexes
with R-P interval equal to PR interval. This excludes si-
nus tachycardia and SART and includes the following
possible arrhythmias:
Regular R-R intervals with retrograde P waves af-
ter the QRS complexes (Fig. 17.33): When R-P inter-
val is shorter than PR interval, the possible arrhythmias
include:
AVRT: (R-P interval 80 milliseconds)
AVNRT: (R-P interval 80 milliseconds)
Junctional tachycardia (paroxysmal or nonparoxys-
mal)
Complete AV dissociation with regular R-R inter-
vals (Fig. 17.34): When there is complete AV dissocia-
tion with regular R-R intervals, AVRT is not possible
and AVNRT is highly unlikely. This is almost always

Lead V1

Figure 17.25: Atrial Tachycardia with 2:1 Atrioventricular Block. The patient is not on digitalis. The atrial
rate is approximately 180 beats per minute and the baseline between the P waves is isoelectric.
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228 Chapter 17

Summary of the Different SVT and Possible Diagnoses

Lead II Possible Diagnoses

Sinus Tachycardia
Sinoatrial Reentrant Tachycardia
Focal Atrial Tachycardia

Focal Atrial Tachycardia

Junctional Tachycardia
Atypical AVNRT
Atypical AVRT

Junctional Tachycardia
AVNRT

AVNRT
Junctional Tachycardia

AVNRT
Junctional Tachycardia

AVRT
AVNRT
Junctional Tachycardia

AVRT
Atrial Flutter with 2:1 AV Block
AVNRT
Focal Atrial Tachycardia
Junctional Tachycardia
Multifocal Atrial Tachycardia
Nonparoxysmal Junctional Tachycardia
with Complete AV Dissociation
Figure 17.26: Different Electrocardio-
gram Patterns of Narrow Complex
Supraventricular Tachycardia in Lead
II. The best possible diagnosis is
highlighted in bold letters and is listed from
top to bottom. The algorithm for diagnosing
narrow complex tachycardia is shown in the
next page. AVNRT, atrioventricular nodal
reentrant tachycardia; AVRT, atrioventricular
reentrant tachycardia.

due to junctional tachycardia with complete AV disso-
ciation.
Junctional tachycardia with complete AV dis-
sociation
Retrograde P Waves with second-degree AV
Wenckebach (Fig. 17.35): This is almost always due
to focal atrial tachycardia. This excludes AVRT and
makes AVNRT highly unlikely.
ECG of Narrow Complex Tachycardia
are the main considerations. Focal atrial tachycardia with vari-
able AV block is also possible although rare.
2. When the R-R interval is regular, the diagnosis of the tachycardia
depends on the location and polarity of the P waves in lead II.
No P waves are present
AVNRT
Junctional tachycardia
If the P waves are upright in lead II, the primary consid-
erations are:
Sinus tachycardia

1. When the R-R interval is irregular, atrial fibrillation, multifo- Focal atrial tachycardia
cal atrial tachycardia, and atrial flutter with variable AV block SART
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Supraventricular Tachycardia due to Altered Automaticity 229

Figure 17.27: Algorithm for Diag- Narrow Complex Tachycardia

nosing Narrow Complex Tachycar-
dia. AVNRT, atrioventricular nodal reen-
trant tachycardia; AVRT, atrioventricular
Irregular R-R Intervals Regular R-R Intervals
reentrant tachycardia.

Multifocal Atrial Tachycardia

Sinus Tachycardia
Atrial Flutter with Variable Block
Atrial Flutter with 2:1 AV Block
Atrial Fibrillation
Supraventricular Tachycardia
Focal Atrial Tachycardia with AV
Block (rare)

P Waves Present P Waves Absent

Sinus Tachycardia AVNRT

Atrial Flutter with 2:1 AV Block Junctional
Supraventricular Tachycardia Tachycardia

P Waves Upright in P Waves are Retrograde

Lead II (Inverted) in Lead II

P Wave in Front of QRS P Wave after QRS

Sinus Tachycardia
Complex or R-P > PR Complex or R-P < PR
Focal Atrial Tachycardia
Sinoatrial Reentrant
Tachycardia
Focal Atrial Tachycardia AVRT
Junctional tachycardia AVNRT
Atypical AVNRT Junctional Tachycardia
Atypical AVRT Atrial Flutter with 2:1 Block
Atrial Flutter with 2:1 Block

2 AV Block or Higher

Focal Atrial Tachycardia

Junctional Tachycardia
Atrial Flutter with Fixed AV Block

Grossly Irregular R-R Intervals

P

MAT

Atrial Fibrillation
Regular Narrow Complex Tachycardia: No P Waves

AVNRT
Atrial Flutter Junctional Tachycardia

Figure 17.28: Narrow Complex Tachycardia with Irreg-
ular R-R Intervals. When the R-R interval in a narrow
complex tachycardia is grossly irregular, the possibilities include
multifocal atrial tachycardia (MAT), atrial fibrillation, and atrial
flutter with variable atrioventricular block.
Figure 17.29: Supraventricular Tachycardia with Reg-
ular R-R intervals and No P Waves. This is commonly
due to atrioventricular nodal reentrant tachycardia. Junctional
tachycardia is another possibility, although this is not as
common.
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230 Chapter 17

Upright P waves in front of the QRS complexes in Lead II

Sinus tachycardia
Focal AT
SART
(Excludes AVNRT and AVRT)

Figure 17.30: Regular R-R Intervals with Upright P

Waves before QRS complexes in Lead II. This is almost
always the result of sinus tachycardia. Focal atrial tachycardia
and sino-atrial reentrant tachycardia are other possibilities.

Retrograde P Waves in Front of QRS Complexes

Focal Atrial Tachycardia

Atypical AVNRT
Atypical AVRT
Junctional Tachycardia
(Excludes Sinus tachycardia and SART)

Figure 17.31: Retrograde P Waves in Front of the QRS Complex. This is

most commonly the result of focal atrial tachycardia. Other possibilities include atyp-
ical atrioventricular nodal reentrant tachycardia, atypical atrioventricular reentrant
tachycardia, and junctional tachycardia, both paroxysmal and nonparoxysmal.

Retrograde P Waves with R-P Interval = PR Interval

Atrial Flutter with 2:1 AV Block

AVRT
Focal Atrial Tachycardia
Atypical AVNRT
Junctional Tachycardia
(Excludes Sinus tachycardia and SART)

Figure 17.32: Retrograde P Waves with R-P Interval Equal to PR

Interval. Atrial flutter with 2:1 AV block is a distinct possibility with the second
flutter wave embedded within the QRS complexes.This can also be due to AVRT,
focal atrial tachycardia, atypical AVNRT and junctional tachycardia both paroxysmal
and nonparoxysmal. AV, atrioventricular; AVNRT, atrioventricular nodal reentrant
tachycardia; AVRT, atrioventricular reentrant tachycardia.

Retrograde P Waves after QRS Complex

AVRT (R-P 80 milliseconds)

AVNRT (R-P <80 milliseconds)
Junctional Tachycardia
0
Focal Atrial Tachycardia with 1 AV Block
R-P Interval

Figure 17.33: Retrograde P Waves with R-P Interval  PR Interval. This

is typically from atrioventricular reentrant tachycardia. Other possibilities include
atrioventricular nodal reentrant tachycardia and junctional tachycardia both parox-
ysmal and nonparoxysmal. Arrow points to the retrograde P wave.

Junctional Tachycardia with

complete AV dissociation. The P
waves are sinus in origin and are
independent from the QRS complex.

Figure 17.34: Junctional Tachycardia with Complete AV Dissociation. The

P waves are upright in lead II and are completely dissociated from the QRS complexes.
The upright P waves represent normal sinus rhythm.
LWBK271-C17_211-232.qxd 29/1/09 7:45 pm Page 231 LWBK270-4119G-C02_073-110.qxd
Supraventricular Tachycardia due to Altered Automaticity
Figure 17.35: Retrograde P waves with Second-Degree
Atrioventricular Wenckebach. This is almost always from focal atrial
tachycardia. Focal junctional tachycardia is also possible, but is unlikely.
If the P waves are retrograde (inverted), the differential
diagnosis revolves around the position of the P waves in
relation to the QRS complexes
Retrograde P waves before the QRS complex with PR
interval 0.12 seconds
n Focal atrial tachycardia
n Atypical AVNRT
n Atypical AVRT
n Junctional tachycardia
n Atrial flutter with 2:1 block
Retrograde P waves before the QRS complex with PR
interval 0.12 seconds
n Junctional tachycardia
n AVNRT (typical and atypical)
n Atypical AVRT
Clinical Implications
Identification of the P wave (or its absence) is crucial to the
diagnosis of narrow complex tachycardia. Several maneuvers
are often helpful in identifying the P waves if they are not ob-
vious in the surface ECG.
Although the P wave should be inspected in all 12
standard leads of the ECG, leads II and V1 are the most
useful. Lead II is very useful, especially in determining
the polarity of the P wave and therefore the origin of the
tachycardia.
The ECG may be magnified to 2 the standard size and
the speed of the recording may be doubled so that the P
waves may be better identified. This maneuver is usually
not very useful unless the voltage of the ECG is small es-
pecially in the limb leads (lead II).
Special leads may be taken (other than the standard 12
leads). These include:
n The left arm electrode can be used as the exploring
electrode and positioned at different areas in the
precordium. The rest of the extremity electrodes re-
tain their usual position. The ECG is recorded in
lead I.
n If this maneuver is not helpful, a Lewis lead can be
recorded by placing the left arm electrode over the
fourth right intercostal space beside the sternum (V1
position) and the right arm electrode at the second
right intercostal space beside the sternum. The ECG is
recorded in lead I.
231
Focal atrial tachycardia
with 2 AV Block
n An esophageal pill electrode can be swallowed and po-
sitioned behind the left atrium. The electrode is con-
nected to a standard precordial lead such as V1.
n Intracardiac recordings may be obtained by inserting
an electrode transvenously into the atria and con-
nected to a standard precordial lead such as V1.
n If a central line is already in place, intracardiac ECG
can be obtained by filling the length of the catheter
with saline. The tip of the central line should be near
or at the right atrium and if multiple catheter lumens
are present, the port closest to the right atrium should
be used. A needle is inserted and left at the injecting
port of the catheter. The needle is connected to V1 or
any precordial lead in the ECG (usually with an alligator
clamp) and recorded in V1.
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Electrocardiogram Findings
Atrial flutter is a supraventricular arrhythmia with a
regular atrial rate of 300  50 beats per minute (Fig. 18.1).
Other features include:
Very regular and uniform flutter waves with a saw
tooth or picket fence appearance.
The flutter waves are typically inverted in leads II,
III, and aVF and upright in V1.
The ventricular rate is variable depending on the
number of atrial impulses conducted through the
atrioventricular (AV) node.
The QRS complexes are narrow unless there is
preexistent bundle branch block or the atrial im-
pulses are conducted aberrantly or through a by-
pass tract.
Atrial flutter is due to reentry within the atria.
There are two types of atrial flutter based on elec-
A.
B.
5 small blocks
1 2 3 4
18
Atrial Flutter
trocardiogram (ECG) presentation: typical and re-
verse typical.
Typical atrial flutter: This is the most common
ECG pattern occurring in 90% of all atrial flutter. In
typical atrial flutter, the atrial impulse travels from
top to bottom across the lateral wall of the right
atrium and circles back from bottom to top across
the atrial septum. The flutter waves are inverted in
lead II and upright in V1 (Fig. 18.2A).
Reverse typical atrial flutter: This type is uncom-
mon occurring only in 10% of cases. The atrial im-
pulse travels down the atrial septum and up the
lateral wall of the right atrium, which is the reverse
of typical atrial flutter. This will cause the flutter
waves to become upright in lead II and inverted in
V1 (Fig. 18.2B).
Atrial rate: The diagnosis of atrial flutter is based on the
atrial rate, which is regular with a sawtooth configuration
and is typically 300  50 beats per minute (bpm). The
Figure 18.1: Atrial Flutter.
(A) Twelve-lead ECG showing atrial
flutter. The flutter waves are regular
with saw tooth or picket fence
appearance and are typically
inverted in leads II, III, and aVF and
upright in V1 (arrows). (B) Lead II is
magnified from the ECG in (A) to
show the appearance of the flutter
waves. There is 4:1 AV conduction,
meaning that there are four flutter
waves (arrows) for every QRS com-
plex. The flutter waves are separated
by five small blocks, which is equiva-
lent to a rate of 300 beats per
minute. ECG, electrocardiogram; AV,
atrioventricular.
233
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234 Chapter 18
Figure 18.2: Diagrammatic A. Typical Atrial Flutter
representation of Atrial
Flutter. (A) Classical atrial flut-
ter with typically inverted flutter
waves in lead II. The impulse
travels down the lateral wall of Right
the right atrium and up the atrial Atrium
septum (arrow) in a counter-
clockwise direction. The reverse
type travels through the same
pathway, (B) down the atrial sep-
tum (arrow) and up the right AV
atrial wall in a clockwise Node
direction, which is the opposite
of classical atrial flutter. This
causes the flutter waves to be
upright in lead II.
Flutter waves inverted in lead II
atrial rate is the most important in differentiating atrial
flutter from the other supraventricular arrhythmias.
The atrial rate is calculated by counting the number
of small boxes between two flutter waves and divid-
ing this number from 1,500 (see Chapter 5, Heart
Rate and Voltage).
The atrial rate in atrial flutter may be 250 bpm if
the patient is taking antiarrhythmic agents that can
slow atrial conduction such as quinidine, sotalol, or
amiodarone.
The baseline between flutter waves is usually wavy
and undulating.
Ventricular rate: Atrial flutter is easy to recognize
when the ventricular rate is slow as when there is 4:1
AV conduction, as shown in Figure 18.1. However,
when the ventricular rate is rapid as when there is 2:1
AV conduction (Fig. 18.3A,B), especially when the QRS
complexes are wide due to bundle branch block (Fig.
18.3C), the flutter waves may be obscured by the QRS
complexes and ST and T waves making atrial flutter
difficult or even impossible to recognize.
Ventricular Rate in Atrial Flutter
The ventricular rate in atrial flutter depends on the
number of atrial impulses that are conducted through
the AV node, thus the ventricular rate can be very rapid
or very slow.
B. Reverse Typical Atrial Flutter
Left Right Left
Atrium Atrium Atrium
AV
Node
Flutter waves upright in lead II
Atrial flutter with 1:1 AV conduction: Atrial flutter
with 1:1 AV conduction is rare but is possible (Fig.
18.4). When atrial flutter with 1:1 AV conduction oc-
curs, every atrial impulse is followed by a QRS com-
plex; therefore, the atrial rate and ventricular rate are
the same and is 300  50 bpm (250 to 350 bpm).
Atrial flutter with 2:1 AV conduction: Atrial flutter
with 2:1 AV conduction (or 2:1 AV block) is the most
common presentation of atrial flutter in the acute setting.
It is also the most difficult to recognize and is the most
commonly overlooked tachycardia with a narrow QRS
complex. Approximately 10% of tachycardia thought to
be SVT is due to atrial flutter. Atrial flutter should always
be distinguished from SVT because the acute treatment
of atrial flutter is different from that of SVT.
When atrial flutter with 2:1 AV block occurs, every
other atrial impulse is followed by a QRS complex, al-
ternating with every other impulse that is not con-
ducted. The ventricular rate is half the atrial rate.
Because the atrial rate is typically 300 bpm, the ventric-
ular rate in atrial flutter with 2:1 conduction is approx-
imately 150 bpm (Fig. 18.5).
Atrial flutter with 2:1 AV block: When there is a reg-
ular tachycardia with narrow QRS complexes and the
ventricular rate is 150 bpm, especially when inverted
P waves are present in lead II, atrial flutter with 2:1
AV block should be the first arrhythmia to consider.
The following examples show some of the difficulties
in recognizing atrial flutter when 2:1 AV block is pres-
ent (Figs. 18.618.8).
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Atrial Flutter 235

A. 5 Atrial rate = 1500/5 = 300 bpm

B.

C.

Figure 18.3: Atrial Flutter. (A) The diagnosis of atrial flutter is based on the presence of flutter waves with typi-
cal saw tooth appearance with a rate of 300  50 beats per minute. The atrial rate is calculated by measuring the
distance between two flutter waves and dividing the number of small blocks from 1500 as shown in (A). When the
ventricular rate is rapid because of 2:1 atrioventricular conduction (marked by the brackets in A and B), especially
when the QRS complexes are wide because of bundle branch block as shown in (C), the diagnosis of atrial flutter is
difficult and may not be possible unless there is slowing of the ventricular rate so that the flutter waves can be rec-
ognized (arrows).

patient may in fact require digitalis or other AV nodal

Atrial Flutter and Supraventricular
Tachycardia
Differentiating atrial flutter from supraventricu-
lar tachycardia (SVT): When the diagnosis of atrial
flutter is uncertain, vagal maneuvers such as carotid si-
nus pressure, is useful in differentiating atrial flutter
from other types of regular narrow complex SVT as
shown (Fig. 18.9).
Atrial flutter: In atrial flutter, carotid sinus pressure
or AV nodal blockers such as adenosine or verapamil
will slow AV nodal conduction resulting in a slower
ventricular rate but will not convert atrial flutter to
normal sinus rhythm (Figs. 18.9 and 18.10).
Regular narrow complex SVT: When the narrow
complex tachycardia is due to SVT, the tachycardia
may convert to normal sinus rhythm with carotid
stimulation. SVT from reentry but not atrial flutter
(Fig. 18.10) is frequently terminated by AV nodal
blockers to normal sinus rhythm (see Chapter 16,
Supraventricular Tachycardia due to Reentry).
Atrial flutter versus atrial tachycardia: Atrial flutter
with 2:1 AV block may be mistaken for atrial tachycar-
dia with 2:1 AV block. Atrial tachycardia with 2:1 AV
block is usually from digitalis toxicity, whereas atrial
flutter with 2:1 AV block is unrelated to digitalis and the
blocking agents to slow down the ventricular rate.
Atrial rate: The atrial rate is the most important fea-
ture in distinguishing atrial flutter from atrial tachycar-
dia (Figs. 18.11 to 18.14). In atrial flutter with 2:1 AV
block, the atrial rate is approximately 300  50 bpm
with the lowest rate at 240 to 250 bpm. In atrial tachy-
cardia with 2:1 AV block, the atrial rate is approxi-
mately 200  50 bpm (150 to 250 bpm) (Fig. 18.11).
Morphology of the P wave: When the atrial rate
of atrial flutter and atrial tachycardia overlaps, the
two arrhythmias may be differentiated by the mor-
phology of the P wave. In atrial flutter, the flutter
waves are typically inverted in leads II, III, and aVF
and the baseline between the QRS complexes is
wavy and undulating (Fig. 18.12). In atrial tachycar-
dia with AV block, the P waves are typically upright
in leads II, III, and aVF and the baseline between the
P waves is isoelectric or flat (Fig. 18.11).
Atrial flutter with variable block: As shown in Fig-
ures 18.15 through 18.17, atrial flutter is easy to recog-
nize when the ventricular rate is slow as when AV con-
duction is 3:1 or higher. In atrial flutter with variable
AV block, the number of flutter waves for every QRS
complex varies from beat to beat (Fig. 18.17).
Atrial flutter with complete AV block: The diagnosis
of complete AV block during atrial flutter should be
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236 Chapter 18

A. Atrial flutter with 1:1 AV conduction

B. Magnified lead II rhythm strip

6 small blocks = 250 bpm

C. Same patient with 2:1 AV conduction

5 small blocks = 300 bpm

Figure 18.4: Atrial Flutter with 1:1 Atrioventricular (AV) Conduction. (AC) From the same patient.
(A, B) Atrial flutter with 1:1 AV conduction. (C) The same patient during 2:1 AV conduction. Arrows point to the
flutter waves, which are typically inverted in lead II with a rate 250 beats per minute.

considered when the ventricular rate is regular and is in
the low 40s, as shown in Figure 18.18. When complete
AV block occurs, the R-R intervals become regular be-
cause of the presence of a ventricular escape rhythm,
independent of the atrial rhythm.
Common Mistakes in Atrial Flutter
Atrial flutter can be confused with other conditions
other than SVT. Although the diagnosis of atrial flutter
is straightforward when the ventricular rate is slow, the
presence of motion artifacts, especially in patients with
tremors such as those with Parkinson disease or pa-
tients receiving intravenous infusion from a volumetric
infusion pump, can be mistaken for flutter waves (Figs.
18.19 to 18.22).
ECG Findings of Atrial Flutter
1. Atrial rate of 300  50 bpm with a minimum atrial rate of 240
to 250 bpm.
2. Very regular and uniform flutter waves with a saw tooth or
picket fence appearance.
3. Flutter waves are typically inverted in leads II, III, and aVF and
upright in V1 in 90% of cases, although this may be reversed in
10% of cases, `becoming upright in leads II, III, and aVF and
inverted in V1.
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Atrial Flutter 237

A. Atrial flutter with 2:1 AV block

1 2

1 2

1 2

B. Atrial flutter with 2:1 AV block

1 2

Figure 18.5: Atrial Flutter with 2:1 Atrioventricular (AV) Block. (A) A 12-lead electrocardiogram showing
atrial flutter with 2:1 AV block. There are two flutter waves for every ventricular complex. The two flutter waves are
identified by the arrows and are labeled 1 and 2. The first flutter wave in lead II (arrow 1) may be mistaken for S wave
and the arrhythmia may be misdiagnosed as SVT. (B) Lead II rhythm strip from (A), which is magnified to show the
flutter waves (arrows).

Lead II: Atrial flutter with 2:1 AV block

1 2

Figure 18.6: Atrial Flutter with 2:1 Atrioventricular Block. The first flutter wave (arrow 1) deforms the ter-
minal portion of the QRS complex and may be mistaken for an S wave. The second flutter wave (arrow 2) is more ob-
vious and precedes the QRS complex but can be mistaken for an inverted P wave. Thus, the arrhythmia can be mis-
taken for supraventricular tachycardia.

Lead II: Atrial flutter with 2:1 AV block

1 2

Figure 18.7: Atrial Flutter with 2:1 Atrioventricular Block. The first flutter wave (arrow 1) may be
mistaken for a depressed ST segment or inverted T wave.
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A. 1
2

B.

Figure 18.8: Atrial Flutter with 2:1 Atrioventricular (AV) Block. The diagnosis of atrial flutter with 2:1 AV block
is not possible in rhythm strip (A). The first flutter wave (arrow 1) is buried within the QRS complex and the second flutter
wave (arrow 2) can be mistaken for an inverted T wave. The diagnosis became evident only after sudden spontaneous
slowing of the ventricular rate (B) (arrows), revealing the classical saw tooth flutter waves between the QRS complexes.

Figure 18.9: Atrial Flutter. When the diagnosis is in doubt, carotid sinus stimulation may slow down the ven-
tricular rate so that the flutter waves (arrows) can be identified. Atrial flutter will not convert to normal sinus rhythm
with carotid sinus pressure or with atrioventricular nodal blockers.

Figure 18.10: Atrial Flutter Resembling Atrioventricular Nodal Reentrant Tachycardia. Leads I, II,
and III are simultaneously recorded. A narrow complex tachycardia with a rate of 125 beats per minute is seen on
the left half of the tracing. The tachycardia was thought to be due to AV nodal reentrant tachycardia because no
obvious P waves were noted. Adenosine was given intravenously, resulting in AV block. Upright flutter waves are
now obvious in leads II and III with a rate of 250 beats per minute (six small blocks). The tachycardia is due to atrial
flutter with 2:1 AV block. AV, atrioventricular.

Upright P waves, rate 200 50 bpm Flat or isoelectric baseline

Figure 18.11: Atrial Tachycardia with 2:1 Atrioventricular Block. The atrial rate is typ-
ically 200  50 beats per minute and the P waves are upright and separated by an isoelectric or
flat line in lead II.
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Inverted flutter waves:

(minimum rate 240-250 bpm) Undulating or wavy baseline

Figure 18.12: Atrial Flutter with 2:1 Atrioventricular Block. In atrial flutter, the atrial
rate is 300  50 beats per minute. The flutter waves are typically inverted in lead II (arrows) and
are separated by a continuously wavy baseline.

Atrial Flutter and Atrial Tachycardia with 2:1 AV Block

Atrial Tachycardia with 2:1 AV Block

Atrial rate approximately 200 50 bpm or 150 - 250 bpm
Upright P waves in lead II
Isoelectric baseline

Lead II

Figure 18.13: Atrial Tachycardia with 2:1 Atrioventricular (AV) Block. Lead II rhythm
strip showing atrial tachycardia with 2:1 AV block with an atrial rate of 230 beats per minute (6.5
small blocks). In atrial tachycardia, the atrial rate is typically 150250 beats per minute. Note also
that the P waves are upright in lead II with an isoelectric baseline. Atrial tachycardia with 2:1 AV
block is usually due to digitalis toxicity and the ST segment depression shown above is
characteristic of digitalis effect.

Atrial Flutter with 2:1 AV Block

Atrial rate approximately 300 50 bpm (minimum rate 240-250 bpm)
Inverted atrial complexes in lead II
Undulating or wavy baseline

A. Before Atrial rate = 1500/6 = 250 bpm

B. After
Atrial rate = 1500/8 = 188 bpm

Figure 18.14: Atrial Flutter (AF) Before and After Administration of

Antiarrhythmic Agent. Lead II rhythm strips from the same patient before (A) and after (B)
giving sotalol orally. The atrial rate in AF can become slower than 240 to 250 beats per minute if
an antiarrhythmic agent is given that can slow the atrial rate. (A) The atrial rate was 250 beats per
minute before receiving sotalol. (B) The atrial rate had decreased to 188 beats per minute after
therapy. The flutter waves retain their typically inverted pattern in lead II, an important feature in
differentiating atrial tachycardia from atrial flutter with 2:1 atrioventricular block.

239
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240 Chapter 18

Figure 18.15: Atrial Flutter with 3:1 Atrioventricular Block. Rhythm strip showing three flutter waves
(arrows) for each QRS complex. The first flutter wave (first arrow) is buried within the QRS complex.

Figure 18.16: Atrial Flutter with 4:1 Atrioventricular Block. There are four flutter waves (arrows) for each
QRS complex.

Figure 18.17: Atrial Flutter with Variable Atrioventricular (AV) Block. The R-R intervals are irregular be-
cause conduction of the atrial impulse across the AV node is variable.

Figure 18.18: Atrial Flutter and Complete Atrioventricular (AV) Block. Lead II rhythm strip showing
atrial flutter with complete AV block. The R-R intervals are regular with a ventricular rate of 33 beats per minute.
The atrial rate is 300 beats per minute.
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Atrial Flutter 241

A.

B.

Figure 18.19: Motion Artifacts Resembling Atrial Flutter. (A, B) From the same patient. (A) Suspicious
atrial flutter although distinct P waves are recognizable before each QRS complex in long lead V5 (arrows). The
repeat electrocardiogram after the electrodes were stabilized (B) distinctly shows that the rhythm is normal sinus
and not atrial flutter.

4. The ventricular rate is variable depending on the number of
atrial impulses conducted through the AV node.
5. The QRS complexes are narrow unless preexistent bundle
branch block is present; the atrial impulses are conducted with
aberration or are conducted through a bypass tract.
Mechanism
Atrial flutter is a reentrant arrhythmia within the atria. It is
usually precipitated by premature atrial complexes or repeti-
tive impulses originating from other areas contiguous to the
atria such as the pulmonary veins.
Typical atrial flutter: The typical form of atrial flutter,
which is the most common presentation, has a reentrant
pathway located within the right atrium. The impulse
travels down the lateral wall and up the atrial septum in a
counterclockwise direction, resulting in negative or in-
verted flutter waves in leads II, III, and aVF and upright
flutter waves in V1. The reentrant circuit involves an area
of slow conduction between the tricuspid orifice and

Figure 18.20: Atrial Flutter due to Motion Artifacts. Another example of atrial flutter due to motion
artifacts is shown. P waves can still be identified preceding each QRS complex (arrows).
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242 Chapter 18

Figure 18.21: Artifacts Resembling Atrial Flutter. The patient was referred with a diagnosis of atrial flutter
based on the electrocardiogram obtained from a doctors office. The tracing shows that there are definite sinus P
waves preceding the QRS complexes especially in leads I, II, and also in V1 to V6 (arrows). The rhythm therefore is not
atrial flutter but normal sinus and the flutter-like undulations seen in leads II, III, and aVF are due to artifacts. Normal
sinus rhythm was verified when the patient arrived for the consultation.

mouth of the inferior vena cava called the cavotricuspid
isthmus. This is the usual site of radiofrequency ablation.
Reverse typical atrial flutter: The other form of atrial
flutter, which is less common, has the same reentrant cir-
cuit but is reversed in direction. The atrial impulse travels
down the atrial septum and up the lateral wall in a clock-
wise direction, resulting in flutter waves that are upright
in leads II, III, and aVF and inverted in V1.
The reentrant circuit in atrial flutter can also occur in other
locations other than the right atrium and includes the left
atrium, in the area of the pulmonary veins, or around a scar
or surgical lesion within the atria. Atrial flutter within the

A. Lead II rhythm strip

B. Lead II rhythm strip

Figure 18.22: Atrial Flutter Caused by Infusion Pump. (A, B) From the same patient. The rhythm strip in
(A) shows artifacts caused by infusion of intravenous fluids using an IVAC volumetric infusion pump. The artifacts
can be mistaken for atrial flutter. The lead II rhythm strip in (B) was taken after the IV infusion pump was discontin-
ued. IV, intravenous.
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left atrium is more difficult to map because of its left atrial
location.
Clinical Significance
The incidence of atrial flutter is variable. It is more common in
men than in women. Although atrial flutter may occasionally
become persistent lasting for days or months, it seldom occurs
as a chronic rhythm, very often converting to normal sinus
rhythm or deteriorating to atrial fibrillation. Atrial flutter and
atrial fibrillation are frequently associated arrhythmias.
Atrial flutter is usually associated with organic or structural
cardiac disease or it may be precipitated by an acute condition.
An acute precipitating cause, usually surgery (cardiac or
noncardiac), pneumonia, acute myocardial infarction, or
congestive heart failure can be identified in 60% of cases.
The remaining cases are associated with chronic cardiac
or pulmonary diseases or hypertension.
Atrial flutter not accompanied by structural cardiac disease
or any precipitating condition is called lone atrial flutter.
Lone atrial flutter is rare occurring only in 1.7% of all cases.
Atrial flutter with a rapid ventricular rate of 150 bpm with
2:1 AV conduction is the most frequent presentation in the
acute setting. Less frequently, it may occur at a slower rate
with a conduction ratio of 4:1. Atrial flutter with an odd con-
duction ratio of 1:1, 3:1, or 5:1 are much less common.
The rapid ventricular rate associated with atrial flutter may oc-
cur in patients with accessory pathways. It can also occur when
there is increased adrenergic activity or when there is thyro-
toxicosis. In patients with atrial fibrillation or atrial flutter who
are being converted to normal sinus with Class IA (quinidine,
procainamide, and disopyramide) and Class IC (propafenone
or flecainide) agents, atrial flutter with 1:1 AV conduction can
occur. Atrial flutter with fast ventricular rate may cause hemo-
dynamic collapse and symptoms of low cardiac output, result-
ing in dizziness or frank syncope especially when there is left
ventricular dysfunction or obstructive valvular disease.
Because atrial flutter follows a fixed pathway within the atria,
the atrial rate is regular and is one of the most regular among
all supraventricular tachyarrhythmias. Atrial flutter with 2:1
AV block may be confused with SVT, especially when one
flutter wave is buried within the QRS complex and the other
flutter wave is inscribed midway between two QRS com-
plexes. The flutter waves can be identified by slowing the ven-
tricular rate with vagal maneuvers or, if unsuccessful, with
AV nodal blocking agents. Adenosine, however, should not
be injected when the tachycardia has wide QRS complexes
because hypotension or ventricular fibrillation may occur if
the tachycardia turns out to be ventricular.
Atrial flutter with 2:1 AV block should be differentiated from
atrial tachycardia with 2:1 AV block. Atrial tachycardia with
2:1 AV block is commonly associated with digitalis toxicity,
whereas atrial flutter with 2:1 block may require more digi-
talis to slow the ventricular rate.
Atrial Flutter 243
Atrial rate: In atrial flutter, the minimum atrial rate is
240 to 250 bpm. In atrial tachycardia with 2:1 AV block,
the atrial rate is usually 200  50 bpm.
Morphology of the P waves: In atrial flutter, the flutter
waves are inverted in II, III, and aVF and the baseline be-
tween the flutter waves is usually wavy and undulating. In
atrial tachycardia with 2:1 AV block, the P waves are up-
right in II, III, and aVF and the baseline between the P
waves is usually isoelectric or flat.
Similar to atrial fibrillation, atrial flutter can cause systemic
thromboembolism and the incidence of stroke approaches
that of atrial fibrillation.
Because atrial flutter is associated with mechanical atrial
contraction, the physical findings of atrial flutter often show
jugular neck vein pulsations coincident with each flutter
wave in the ECG. Thus, the number of atrial pulsations (A
waves) will be faster than the ventricular rate because atrial
flutter is usually associated with AV block. When there is
variable AV block, an irregular heart rate will be present,
which can be mistaken for atrial fibrillation. The intensity of
the first heart sound is constant when the AV block is fixed
but is variable when there is varying AV conduction.
Therapy
In patients who are hemodynamically unstable and are hy-
potensive with low cardiac output, immediate direct current
cardioversion is indicated and receives a Class I recommenda-
tion according to the 2003 American College of Cardiology/
American Heart Association Task Force on Practice Guide-
lines, and the European Society of Cardiology practice guide-
lines for the management of patients with supraventricular
arrhythmias. Immediate cardioversion is also indicated
among stable patients and also carries a Class I recommenda-
tion since atrial flutter can be easily converted to normal sinus
rhythm with low energy settings of 50 joules or less using
monophasic shocks. Therapy of atrial flutter is similar to that
of atrial fibrillation and includes three considerations:
Anticoagulation to prevent thromboembolism
Control of ventricular rate
Conversion of atrial flutter to normal sinus rhythm
Anticoagulation to prevent thromboembolism: Antico-
agulation should always be considered in all patients if the
duration of atrial flutter is 48 hours or the duration is not
definitely known. Atrial flutter, similar to atrial fibrillation, is
associated with increased incidence of thromboembolism.
This is further discussed in Chapter 19, Atrial Fibrillation.
Control of ventricular rate: Control of ventricular rate in
atrial flutter is frequently more difficult than control of ven-
tricular rate in atrial fibrillation. The pharmacologic agents
that are commonly used include AV nodal blocking agents
such as calcium channel blockers (verapamil or diltiazem),
beta blockers, digitalis, and amiodarone. The agent of choice
depends on the clinical status of the patient. The following
are the recommendations for control of ventricular rate in
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244 Chapter 18
patients with atrial flutter according to the 2003 American
College of Cardiology/American Heart Association Task Force
on Practice Guidelines, and the European Society of Cardiol-
ogy practice guidelines for supraventricular arrhythmias.
Poorly tolerated: If the arrhythmia is poorly tolerated,
direct current cardioversion to convert atrial flutter to
normal sinus rhythm is a Class I recommendation. The
use of nondihydropyridine calcium channel blockers (ve-
rapamil, diltiazem) or beta blockers (metoprolol, propra-
nolol, or esmolol) are the most useful and effective agents
in controlling ventricular rate in atrial flutter and receive
a Class IIa recommendation. The beta blockers and cal-
cium channel blockers have the same efficacy in slowing
the ventricular rate. These agents are more effective than
digitalis or amiodarone. Calcium blockers and beta
blockers should not be used when there is acute decom-
pensated heart failure or when the patient is hypotensive.
Intravenous digoxin or amiodarone are the preferred
agents and receive a Class IIb recommendation.
Stable patients: Conversion of atrial flutter to normal
sinus rhythm with direct current cardioversion or with
the use of atrial or transesophageal pacing both receive
Class I recommendation even among stable patients. Cal-
cium channel blockers and beta blockers are the most ef-
fective agents and receive Class I recommendation for
control of ventricular rate in atrial flutter. Digitalis and
amiodarone are less effective and receive a Class IIb rec-
ommendation.
Conversion of atrial flutter to normal sinus rhythm: AV
nodal blockers, such as calcium channel blockers, beta block-
ers, and digoxin can slow AV conduction and control the
ventricular rate, but are not effective in converting atrial flut-
ter to normal sinus rhythm. Conversion of atrial flutter to
normal sinus rhythm can be accomplished by the following:
Antiarrhythmic agents
Rapid atrial pacing
Electrical cardioversion
Catheter ablation
Antitachycardia devices
Surgery
Antiarrhythmic agents: The use of antiarrhythmic agents
in converting atrial flutter to normal sinus rhythm is re-
served for stable patients. The following antiarrhythmic
agents are effective in converting atrial flutter to normal si-
nus rhythm: Class IA antiarrhythmic agents (pro-
cainamide), Class IC (flecainide and propafenone), and
Class III agents (amiodarone, ibutilide and sotalol). Among
the antiarrhythmic agents mentioned, the only intravenous
agents available in the United States are ibutilide, amio-
darone, and procainamide.
Ibutilide: Ibutilide, a Class III antiarrhythmic agent, is
the most effective in acutely converting atrial flutter to
normal sinus rhythm. This agent receives a Class IIa rec-
ommendation in converting stable patients with atrial
flutter to normal sinus rhythm. Up to 78% of atrial flutter
will convert to normal sinus rhythm within 90 minutes of
infusion. The drug is less effective in converting atrial fib-
rillation to normal sinus rhythm. For patients weighing
60 kg, an initial 1 mg dose is injected intravenously for
10 minutes. The same dose may be repeated after 10 min-
utes if the initial 1 mg bolus is not effective. Torsades de
pointes can occur in 2% to 4% of cases. The drug should
not be given if the QTc is prolonged, there is sick sinus
syndrome, or left ventricular dysfunction.
Procainamide: Procainamide, a Class IA antiarrhythmic
agent, is given intravenously with a loading dose of 10 to
14 mg/kg for 30 minutes. This is followed by a mainte-
nance infusion of 1 to 4 mg/minute. Procainamide should
be combined with AV nodal blocking agents because 1:1
AV conduction can occur during infusion. This agent re-
ceives a Class IIb recommendation for converting stable
patients with atrial flutter to normal sinus rhythm.
Amiodarone: Amiodarone, a Class III antiarrhythmic
agent, is effective in converting atrial flutter to normal
sinus rhythm. It is also effective in controlling the ven-
tricular rate of atrial flutter. The agent is not as effective
as ibutilide, but is the least proarrhythmic and the drug
of choice when left ventricular dysfunction is present.
The dose of amiodarone for terminating atrial flutter is
5 mg/kg given intravenously in 10 minutes. This drug
receives a Class IIb recommendation for both rate con-
trol and for conversion of atrial flutter to normal sinus
rhythm.
Other agents: Propafenone and flecainide (Class IC
agents) and sotalol (Class III agent) are not available as in-
travenous agents in the United States. Dosing is discussed
in Chapter 19, Atrial Fibrillation. These agents receive a
Class IIb recommendation for conversion of atrial flutter
to normal sinus rhythm. Class IC agents should be com-
bined with AV nodal blocking agents to prevent 1:1 AV
conduction.
Rapid atrial pacing: Although electrical cardioversion is
very effective in converting atrial flutter to normal sinus
rhythm, rapid atrial pacing may be preferable to electrical
cardioversion since rapid atrial pacing does not require in-
travenous sedation. Among stable patients, atrial or trans-
esophageal pacing carries a Class I recommendation for con-
verting atrial flutter to normal sinus rhythm. Rapid atrial
pacing is performed by introducing an electrode catheter
transvenously into the right atrium. It can also be performed
transesophageally by swallowing a pill electrode positioned
behind the left atrium. The pacemaker impulse may be able
to block the reentrant circuit causing the arrhythmia to ter-
minate. Atrial fibrillation may develop during rapid atrial
pacing, which is much easier to control with AV nodal block-
ing agents and is a more acceptable arrhythmia than atrial
flutter. Conversion of atrial flutter to atrial fibrillation is con-
sidered a favorable outcome of atrial pacing. Atrial fibrilla-
tion may initially occur during transition from atrial flutter
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to normal sinus rhythm. There are two types of atrial flutter
based on response to rapid atrial pacing:
Type I. Atrial flutter is called type I if it can be converted
to normal sinus rhythm with rapid atrial pacing. The
atrial rate in type I atrial flutter is classically 240 bpm
and includes both typical and reverse typical atrial flutter
as well as atrial flutter associated with reentry around sur-
gical lesions within the atria.
Type II. Atrial flutter is called type II when it can not be in-
terrupted by rapid atrial pacing. The atrial rate is more rapid
than type I atrial flutter and exceeds 340 beats per minute.
Electrical cardioversion. Atrial flutter is one of the most
responsive arrhythmias that can be terminated successfully
with very low energy settings. Approximately 25 to 50 joules
or less may be enough to terminate atrial flutter especially if
biphasic current is used. Fifty to 100 joules is usually needed
during elective cardioversion and is effective in 95% of pa-
tients. Direct current cardioversion is the treatment of choice
when rapid conversion to normal sinus rhythm is desired
and receives a Class I recommendation for both stable and
unstable patients.
Catheter ablation of the reentrant pathway: Long-term
therapy of atrial flutter especially when recurrent includes abla-
tion of the reentrant pathway with an endocardial catheter. In
typical atrial flutter, the reentry is confined to the right atrium
and part of the pathway involves an area between the tricuspid
orifice and mouth of the inferior vena cava called the cavotri-
cuspid isthmus. This is the area where the reentrant circuit is
usually interrupted by radiofrequency ablation.
Antitachycardia devices: Permanent pacemakers are capa-
ble of delivering rapid atrial pacing and can be implanted in
patients who are responsive to rapid atrial pacing. Devices
capable of delivering shocks within the atrium are also capa-
ble of converting atrial flutter to normal sinus rhythm. These
devices, however, are currently not available for clinical use.
Surgery: This is similar to radiofrequency ablation except
that surgery is performed to ablate the reentrant circuit. This
approach is feasible in patients who are also scheduled to un-
dergo coronary bypass surgery or open heart surgery for
valvular disease.
Prognosis
Unlike atrial fibrillation, atrial flutter does not continue in-
definitely and usually lasts only for a few days or a few weeks,
Atrial Flutter 245
although atrial flutter have been documented to last for sev-
eral years. Atrial flutter usually degenerates to atrial fibrilla-
tion. It can result in tachycardia-mediated cardiomyopathy if
the ventricular rate is not controlled. It may also cause
thromboembolic events similar to atrial fibrillation.
Atrial flutter is usually associated with cardiac or pulmonary
disease or an acute precipitating event. Unlike lone atrial fib-
rillation where 10% to 30% of patients do not have associ-
ated cardiac or pulmonary disease, lone atrial flutter is rare.
The prognosis of atrial flutter therefore depends on the un-
derlying condition.
Suggested Readings
Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
ACC/AHA/ESC guidelines for the management of patients
with supraventricular arrhythmiasexecutive summary. A
report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines, and the
European Society of Cardiology Committee for Practice
Guidelines (Writing Committee to Develop Guidelines for
the Management of Patients with Supraventricular Arrhyth-
mias). J Am Coll Cardiol. 2003;42:14931531.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006
Guidelines for the management of patients with atrial fibril-
lation: A report of the American College of Cardiology/
American Heart Association Task Force on Practice Guide-
lines and the European Society of Cardiology Committee for
Practice Guidelines (Writing Committee to Revise 2001
Guidelines for the Management of Patients with Atrial Fib-
rillation). J Am Coll Cardiol. 2006;48:e149e246.
Ghali WA, Wasil BI, Brant R, et al. Atrial flutter and the risk of
thromboembolism: a systematic review and meta-analysis.
Am J Med. 2005;118:101107.
Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter
and regular atrial tachycardia according to electrophysiolog-
ical mechanisms and anatomical basis. A statement from a
joint expert group from the working group of arrhythmias of
the European Society of Cardiology and the North American
Society of Pacing and Electrophysiology. Eur Heart J. 2001;
22:11621182.
Waldo AL, Biblo LA. Atrioventricular nodal-independent
supraventricular tachycardias. In: Topol E, ed. Textbook in
Cardiovascular Medicine. 2nd ed. Philadelphia: Lippincott
Williams & Wilkins; 2002:14291451.
Wellens HJJ. Contemporary management of atrial flutter. Circu-
lation. 2002:106:649652.
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19
Atrial Fibrillation

Fibrillatory waves may not be present. Instead, a flat

Electrocardiogram Findings
Prevalence: Atrial fibrillation (AF) is the most com-
mon sustained arrhythmia that one encounters in clin-
ical practice. It accounts for approximately one third of
all hospitalizations from cardiac arrhythmias. In the
general population, approximately 2.2 million Ameri-
cans or 1% have AF; however, the prevalence varies
according to the age group and is higher in the elderly.
AF is rare in children and young adults.
It is also rare in individuals younger than age 60
years because 1% of the population in this age
group has AF.
Atrial Fibrillation
It increases to more than 8% among patients older
than 80 years of age.
The median age of patients with AF is approxi-
mately 75 years.
Electrocardiogram (ECG) findings: AF is a common
cause of stroke in the elderly. AF therefore should be
recognized because the risk of stroke can be minimized
if the arrhythmia is treated appropriately. The follow-
ing are the ECG features of AF.
Presence of very irregular and disorganized atrial
Ventricular Rate
activity represented in the ECG as fibrillatory waves.
These fibrillatory waves, also called F waves, are
due to several independent reentrant wavelets
within the atria (Fig. 19.1).
The fibrillatory waves may be fine or coarse and
have varying morphologies, which can be mistaken
for P waves.
line with irregularly irregular R-R intervals may be
present.
The atrial rate in AF is 350 beats per minute (bpm).
The ventricular rate is irregularly irregular and de-
pends on the number of atrial impulses conducted
through the atrioventricular (AV) node.
The QRS complexes are narrow unless there is
bundle branch block, aberrant conduction, or pre-
excitation.
Atrial rate: There are no distinct P waves in AF. In-
stead, fibrillatory or F waves are present with a rate that
exceeds 350 bpm. The F waves vary in size and shape
and may be coarse or fine or, in some instances, it may
not be visible in any lead of a complete 12-lead ECG.
When fibrillatory waves are not visible, the diagnosis of
AF is based on the presence of irregularly irregular R-R
intervals as shown (Fig. 19.2B).
Ventricular rate: The ventricular response during AF
is irregularly irregular and the rate will depend on the
state of the AV node. When there is heightened parasym-
pathetic activity or AV nodal disease, the ventricular rate
may be very slow. Conversely, when there increased
sympathetic activity, the ventricular rate may be very

Lead II

Figure 19.1: Atrial Fibrillation. Rhythm strip showing atrial fibrillation. Note the presence of fibrillatory waves
(arrows) between irregularly irregular R-R intervals.

246
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Atrial Fibrillation 247

A.

B.

Figure 19.2: Atrial Fibrillation. Two different ECGs are shown. (A) AF with fibrillatory waves in V1 and in
several other leads marked by the arrows. (B) Twelve-lead ECG from another patient with AF showing absence of
atrial activity with virtually no fibrillatory waves in the whole tracing. The diagnosis of AF is based on the presence
of irregularly irregular R-R intervals. AF, atrial fibrillation; ECG, electrocardiogram.

rapid. Because the ventricular rate in AF is irregularly Ten seconds: If the heart rate is very slow, a longer
irregular, the heart rate should be calculated using a interval such as 10 seconds is measured. This is equiv-
long lead rhythm strip rather than using only the dis- alent to 50 large blocks (Fig. 19.4). The number of
tance between two QRS complexes, as shown in the fol- QRS complexes counted within the 10-second inter-
lowing section. val multiplied by 6 is the heart rate per minute. Again,
Six second time lines: If 3-second time lines are the first QRS complex is not counted.
present in the ECG monitor strip, 6 seconds can be
easily measured. This is equivalent to 30 large blocks
in the ECG paper (Fig. 19.3). The number of QRS
complexes are counted inside the 6-second time line
The Ventricular Rate in AF
and multiplied by 10 to give the heart rate per
minute. The first QRS complex is not counted be- The ventricular rate during AF can be slow or rapid as
cause this serves as baseline. shown in Figs. 19.5A-E. When the ventricular rate is
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248 Chapter 19

6 Seconds (30 large blocks)

Heart Rate = 10.5 10 = 105 bpm

0 1 2 3 4 5 6 7 8 9 10

Figure 19.3: Six-Second Markers. Thirty large blocks is equivalent to 6 seconds. In this ex-
ample, there are 10.5 QRS complexes within the 6-second time markers, thus the heart rate is
10.5  10  105 beats per minute.

slow (Figs. 19.5AC), AF can be easily recognized.
However, when the ventricular rate is faster (Fig.
19.5D,E), AF is more difficult to diagnose because the
QRS complexes are clustered together and the undulat-
ing baseline and irregularly irregular R-R intervals be-
come more difficult to evaluate.
Clinical Classification of AF
Classification: AF may be classified according to its
clinical rather than its electrocardiographic presenta-
tion. The American College of Cardiology/American
Heart Association Task Force on Practice Guidelines,
and the European Society of Cardiology Committee
(ACC/AHA/ESC) 2006 guidelines for the management
of AF identify several types of AF.
Nonvalvular AF: AF is considered nonvalvular when
it occurs in the absence of rheumatic mitral valve dis-
ease, prosthetic heart valve, or mitral valve repair.
Valvular AF: AF is considered valvular when it is as-
sociated with rheumatic mitral stenosis, prosthetic
heart valve, or the patient has previously undergone
valve repair.
Lone AF: AF occurring in individuals 60 years of
age with structurally normal hearts and no evidence
of pulmonary disease. These individuals are not hy-
pertensive and have no clinical or echocardio-
graphic evidence of cardiac or pulmonary disease.
These patients are important to identify because
they are low risk for thromboembolism.
First detected: As the name implies, AF is detected
for the first time, regardless of duration or previous
episodes. A number of patients with first-detected
AF have the potential to revert to normal sinus
rhythm spontaneously.
Recurrent: AF is recurrent if two or more episodes
have occurred. The AF may be paroxysmal or per-
sistent.
Paroxysmal: When recurrent AF has sudden onset
and abrupt termination. The episodes are usually
self terminating lasting for 7 days with most
episodes lasting 2 hours.
Persistent: AF is persistent if the arrhythmia is more
than 7 days in duration. This also includes AF of much
longer duration, including those lasting for more than
1 year. In persistent AF, the episodes are no longer self
terminating, although the AF can be terminated with
pharmacologic agents or with electrical cardioversion.
Permanent: AF is permanent if the arrhythmia can
no longer be converted to normal sinus rhythm with
electrical cardioversion or pharmacologic agents.
The arrhythmia is usually persistent, lasting 1 year,
or a previous electrical cardioversion has failed.
Associated diseases: The most common diseases asso-
ciated with AF include hypertension, ischemic heart dis-
ease, heart failure, valvular diseases, and diabetes mellitus.
Mechanism: AF is a reentrant arrhythmia character-
ized by the presence of multiple independent reentrant
wavelets within the atria (Fig. 19.6). The fibrillatory
waves have a rate of 350 bpm. These fibrillatory waves
are often precipitated by premature atrial complexes

10 Seconds (50 large blocks)

Heart Rate = 7 6 = 42 bpm

0 1 2 3 4 5 6 7

Figure 19.4: Ten-Second Markers. When the heart rate is very slow, 10 seconds is a more
accurate marker. This is equivalent to 50 large blocks. In the above example, there are seven QRS
complexes within the 10-second time marks. The heart rate is 7  6  42 beats per minute.
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Atrial Fibrillation 249

A. Heart Rate = 3 10 = 32 beats per minute (bpm) Figure 19.5: Atrial Fibrilla-
6s tion (AF). AF is usually recog-
nized by the irregularly irregular
R-R intervals and undulating
baseline. As the ventricular rate
becomes faster (AE), the R-R
B. Heart Rate = 5 complexes 12 = 63 bpm
intervals become less irregular.
5s The ventricular rate in rhythm
strip (E) is so rapid that the R-R
interval almost looks regular and
can be mistaken for supraventric-
ular tachycardia instead of AF.
C. Heart Rate = 7 complexes 12 = 84 bpm
5s

D. Heart Rate = 10 15 = 150 bpm

4s

E. Heart Rate = 9 20 = 180 bpm

3s

originating from the atrial wall or crista terminalis

(Fig. 19.7). More recently, it has been shown that AF
can also be initiated by repetitive firing of automatic
foci within the pulmonary veins. These rapidly firing
automatic foci may occur in one or more pulmonary
veins. They cannot be recorded in the surface ECG, but
can be recorded with intracardiac techniques. These
ectopic impulses can also originate from large veins
draining into the atria, including the superior vena
cava and coronary sinus, and can precipitate AF when
there is appropriate substrate for reentry.
Common Mistakes in AF
Atrial fibrillation can be mistaken for supraven-
tricular tachycardia: As previously mentioned, when
the ventricular rate is unusually rapid, the R-R interval
may look regular because the QRS complexes are clus-
tered very close together. Thus, AF with a very rapid
ventricular rate can be mistaken for supraventricular
tachycardia (Fig. 19.8). The diagnosis of AF can be as-
certained by slowing the ventricular rate with vagal

Sinus Figure 19.6:Diagrammatic

Node Representation of Atrial Fibrillation (AF).
Multiple independent
AF is a reentrant arrhythmia characterized by the
wavelets in the atria
presence of multiple independent wavelets
within the atria with an atrial rate of 350 beats
AV Node per minute. These reentrant wavelets can be pre-
cipitated by ectopic impulses originating from the
Bundle of His
pulmonary veins as well as other large veins
Bundle Branches draining into the atria.

Ventricles
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250 Chapter 19

Figure 19.7: Premature Atrial Complex (PAC) Precipitating Atrial Fibrillation. Rhythm strip showing a
single PAC (arrow) precipitating atrial fibrillation. The rhythm strips are continuous.

maneuvers such as carotid sinus pressure. When carotid
sinus pressure is applied, an irregularly irregular R-R
interval with fibrillatory or undulating baseline can be
demonstrated between the QRS complexes (Fig. 19.9).
AF can be mistaken for multifocal atrial tachycar-
dia: The fibrillatory waves, especially when they are
coarse, may be mistaken for P waves. Some of these fib-
rillatory or F waves may be inscribed before the QRS
complexes. When this occurs, AF may be mistaken for
multifocal atrial tachycardia (Fig. 19.10). In multifocal
atrial tachycardia, anticoagulation is not necessary be-
cause this arrhythmia is not associated with increased
risk of thromboembolic events, whereas in AF, antico-
agulation is standard therapy for the prevention of
stroke, especially in high-risk patients.
AF may be diagnosed even when fibrillatory waves are
absent by the irregularly irregular R-R intervals (Fig.
19.11). However, in patients with permanently im-
planted ventricular pacemakers (Fig. 19.12), patients
with complete AV dissociation (Fig. 19.13), or com-
plete AV block (Fig. 19.14), the R-R intervals may be-
come completely regular. If there are no fibrillatory
waves present, the diagnosis of AF may be missed com-
pletely. Patients with unrecognized AF are at risk for
stroke as these patients will not be treated appropriately.
AF with regular R-R intervals: The ventricular rate in
AF is irregularly irregular. The ventricular rate can be-
come regular when there is complete AV dissociation
or complete AV block.
Complete AV dissociation: AF with complete AV
dissociation is frequently due to digitalis toxicity.
Digitalis blocks the AV node and excites the AV
junction and ventricles resulting in junctional or
ventricular ectopic rhythms. AF with an irregularly
irregular R-R interval that suddenly becomes regu-
lar may be due to digitalis toxicity (Fig. 19.13). In
complete AV dissociation, the ventricles are no
longer controlled by the AF, but rather by a separate

Figure 19.8: Atrial Fibrillation with Rapid Ventricular Response. When the ventricular rate is very
rapid, the irregularity in the R-R intervals may not be obvious. The arrhythmia can be mistaken for supraventricular
tachycardia especially when F waves are not grossly apparent. Note, however, that the R-R intervals are not regular.
Carotid sinus stimulation may be helpful in establishing the diagnosis.
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Atrial Fibrillation 251

Carotid Sinus Stimulation

Figure 19.9: Carotid Sinus Stimulation. The rhythm looks regular and can be mistaken
for supraventricular tachycardia. When the diagnosis of AF is in doubt, carotid sinus stimulation
may be helpful in differentiating AF from other narrow complex supraventricular arrhythmias.
Carotid sinus stimulation (arrow) causes slowing of the ventricular rate resulting in prolongation
of the R-R interval. This will allow identification of a wavy baseline representing the fibrillating
atria. AF, atrial fibrillation.

Figure 19.10: Atrial Fibrillation (AF). The coarse F waves may be mistaken for P waves (arrows) and AF may
be misdiagnosed as multifocal atrial tachycardia.

Figure 19.11: Atrial Fibrillation (AF). Even in the absence of fibrillatory waves between QRS complexes, AF
may be diagnosed by the irregularly irregular R-R intervals as shown (above). However, when the R-R intervals are
regular (below) the diagnosis of AF may be difficult.

Figure 19.12: Atrial Fibrillation. The presence of atrial fibrillation may be difficult to diagnose in a patient
with a ventricular pacemaker if there are no fibrillatory waves in baseline electrocardiogram as shown. The presence
of atrial fibrillation was suspected only after the patient sustained a transient ischemic attack.

Figure 19.13: Atrial Fibrillation (AF) with Complete Atrioventricular (AV) Dissociation. This patient
with known chronic AF suddenly developed regular R-R intervals because of AV dissociation. When the ventricular
rate in atrial fibrillation suddenly regularizes, the etiology is usually digitalis toxicity.
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252 Chapter 19

Figure 19.14: Atrial Fibrillation (AF) and Complete Atrioventricular (AV) Block. The rhythm is AF
although the R-R intervals are regular. The QRS complexes are wide with a very slow rate of approximately 33 beats
per minute. The rhythm is AF with complete AV block.

pacemaker, usually the AV junction with a regular
rate that exceeds 60 bpm.
Complete AV Block: When there is complete AV
block, the atrial fibrillatory impulses will not be able
to conduct to the ventricles. An AV junctional or
ventricular escape rhythm usually comes to the res-
cue; otherwise, the ventricles will become asystolic.
In complete AV block, the ventricular rate is slow and
regular usually in the mid to low 40s (Fig. 19.14).
Aberrant ventricular conduction mistaken for
premature ventricular complex: Premature atrial
impulses are normally conducted to the ventricles with
narrow QRS complexes very similar to a normal sinus
impulse. If the impulse is too premature, it may find
one of the bundle branches still refractory from the
previous impulse and will be conducted with a wide
QRS complex. These premature atrial impulses that are
followed by wide QRS complexes are aberrantly con-
ducted impulses, which can be mistaken for premature
ventricular complex. Aberrantly conducted atrial im-
pulses usually have right bundle branch block configu-
ration with rSR pattern in V1 because the right bundle
branch has a longer refractory period than the left bun-
dle branch in most individuals.
Ashman phenomenon: In AF, the R-R intervals are
irregularly irregular. Some R-R intervals are longer and
other R-R intervals are shorter. When the R-R intervals
are longer or the heart rate is slower, the refractory pe-
riod of the conduction tissues becomes longer. When
the R-R intervals are shorter or the heart rate is faster,
the refractory period is shorter. If a long R-R interval is
followed by a short R-R interval (long/short cycle), the
atrial impulse may find the right bundle branch still re-
fractory from the previous impulse and will be con-
ducted with a wide QRS complex. This aberrantly con-
ducted complex is the second complex (the complex
with a short cycle following a long cycle), as shown in
Figure 19.15. This variability in the refractory period of

Long cycle Short cycle

Aberrantly
Conducted
complex

Figure 19.15: Ventricular Aberration. Arrow pointing up shows an aberrantly conducted

supraventricular impulse, which is the second QRS complex after a long R-R interval. Aberrantly
conducted complexes are wide usually with a right bundle branch block pattern. The wide QRS
complex can be easily mistaken for a premature ventricular complex.
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Figure 19.16: Atrial Fibrillation (AF) and Wolff-Parkinson-White (WPW) Syndrome. Note the
presence of irregularly irregular R-R intervals with very bizarre QRS complexes because of AF with varying degrees
of ventricular fusion. AF occurring in the presence of WPW syndrome may result in hemodynamic instability and
sudden cardiac death due to ventricular fibrillation.
the conduction system during long/short cycles in AF
is called the Ashman phenomenon.
Atrial Fibrillation and Wolff-Parkinson-
White Syndrome
Atrial fibrillation and Wolff-Parkinson-White (WPW)
syndrome: The most dreadful complication of AF can
occur in patients with WPW syndrome (see Chapter
20, Wolff-Parkinson-White Syndrome). In WPW syn-
drome, an accessory pathway connects the atrium di-
rectly to the ventricles; thus, the atrial impulse can
reach the ventricles not only through the AV node but
also through the bypass tract. AF associated with a by-
pass tract can deteriorate to ventricular fibrillation and
can cause sudden cardiac death (Fig. 19.16).
Unlike the AV node, which consists of special cells
with long refractory periods, the bypass tract con-
sists of ordinary working myocardium with much
shorter refractory period. Thus, during atrial flutter
(atrial rate 250 bpm) or AF (atrial rate 350
bpm), the rapid atrial impulses which are normally
delayed or blocked at the AV node due to its longer
refractory period, may be conducted directly to the
ventricles through the bypass tract resulting in very
rapid ventricular rate.
AV nodal blocking agents are standard drugs for
controlling the ventricular rate in AF. These drugs
Atrial Fibrillation 253
are contraindicated when there is WPW syndrome
because they enhance conduction across the bypass
tract resulting in rapid ventricular rate and hemo-
dynamic collapse (see Chapter 20, Wolff-Parkinson-
White Syndrome).
ECG Findings
1. Fibrillatory waves are present in baseline ECG representing
disorganized atrial activity.
2. The R-R intervals are irregularly irregular.
3. The ventricular rate is variable and depends on the number of
atrial impulses conducted through the AV node. In younger
individuals, the ventricular rate is faster and usually varies
from 120 to 150 bpm, but is slower in older individuals.
4. The QRS complexes are narrow unless there is preexistent
bundle branch block, ventricular aberration, or preexcitation.
Mechanism
In AF, multiple independent reentrant wavelets are present
within the atria. These reentrant wavelets may be precipi-
tated by premature atrial complexes or spontaneous depolar-
izations originating from pulmonary veins as well as other
large veins draining into the atria.
For AF to become sustained, the atria is usually enlarged and
structural changes such as scarring and fibrosis are usually
present. These structural changes in the atria provide a sub-
strate for reentry.
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254 Chapter 19
Clinical Significance
The prevalence of AF increases with age. At age 50, approxi-
mately 0.5% have AF. This increases to more than 8% by age
80 years. The median age of a patient with AF is 75 years. The
incidence of AF is higher among patients with congestive
heart failure and high blood pressure, which can be reduced
with angiotensin-converting enzyme inhibitors or with an-
giotensin receptor blockers.
AF and atrial flutter are the only two arrhythmias that in-
crease the risk for stroke and thromboembolism. The throm-
bus is usually located in the left atrial appendage. Thrombus
confined to the left atrial appendage can not be diagnosed by
transthoracic echocardiography. Transesophageal echo is the
best imaging modality that can detect a left atrial appendage
thrombus.
Valvular AF: Valvular AF includes patients with AF associated
with rheumatic mitral valve disease, especially those with mi-
tral stenosis and patients with prosthetic mitral valve or previ-
ous mitral valve repair. These patients are high risk for stroke
and should be adequately anticoagulated with warfarin.
Nonvalvular AF: Patients with AF who do not have any of
these features have nonvalvular AF. The risk of stroke for pa-
tients with nonvalvular AF is low unless they have markers
that increase their risk for thromboembolism. These markers
come under the eponym of CHADS2 (Cardiac failure, Hy-
pertension, Age 75 years, Diabetes, and Stroke). History of
stroke or previous transient ischemic attack carries a risk that
is twice that of the other risks features, thus a factor of 2 is
added under Stroke.
Lone AF: When AF is not associated with any known cause
or any evidence of cardiopulmonary disease in a patient
younger than 60 years of age, lone AF is present. This is seen
in up to 20% to 25% of all patients with persistent AF.
Patients with lone AF should be identified because these pa-
tients are low risk for thromboembolism.
AF may be reversible and transient when it occurs acutely in
the setting of pneumonia or other acute respiratory infec-
tions, acute myocarditis, pericarditis, thyrotoxicosis, pul-
monary embolism, acute myocardial infarction, or after car-
diac or noncardiac surgery. It may also be precipitated by
excess intake of alcohol often called holiday heart syndrome
and other metabolic abnormalities. AF may spontaneously
convert to normal sinus rhythm if the cause is reversible
and may not recur when these conditions are corrected or
stabilized.
Symptoms of AF may vary from a completely asymptomatic
patient to one with frank syncope. When the ventricular rate
is unusually rapid exceeding 150 bpm, symptoms of hy-
potension, dizziness, even frank syncope, congestive heart
failure, or myocardial ischemia may occur because of de-
creased cardiac output. The decreased cardiac output is due
to loss of atrial contribution to left ventricular (LV) filling.
The rapid ventricular rate also shortens diastole further de-
creasing ventricular filling.
AF can cause tachycardia mediated cardiomyopathy. It may
precipitate heart failure and pulmonary edema in patients
with LV dysfunction and stenotic valves including mitral
stenosis especially when the ventricular rate is not controlled.
When AF is present, the most common underlying abnor-
mality is usually hypertension or coronary artery disease.
Other frequent underlying conditions associated with AF in-
clude cardiomyopathy, hyperthyroidism, valvular heart dis-
ease (especially mitral stenosis or insufficiency), chronic ob-
structive pulmonary disease, and pericarditis.
Congestive heart failure, regardless of etiology, is now in-
creasingly recognized as a cause of AF. The use of an-
giotensin-converting enzyme inhibitors and blockers of the
renin-angiotensin aldosterone system has been shown to de-
crease the incidence of AF in patients with heart failure as
well as in patients with high blood pressure, especially those
with LV hypertrophy.
The physical findings in AF include:
Disappearance of the jugular A waves in the neck be-
cause of the loss of normal sinus rhythm
Absence of fourth heart sound
Varying intensity of the first heart sound because of the
varying R-R intervals. When the R-R interval is pro-
longed, the intensity of the first heart sound is softer.
When the R-R interval is short, the intensity of the first
heart sound is louder.
When a systolic murmur is present, AF may be useful in
differentiating whether the heart murmur is outflow (aortic
stenosis or functional murmur) or inflow (mitral regurgita-
tion) in origin. If the intensity of the murmur increases after
a long R-R interval, the murmur is outflow in origin. If the
intensity of the murmur does not change following a long
R-R interval, the murmur is due to mitral regurgitation.
Treatment
Treatment of AF is similar to that of atrial flutter and revolves
around three conditions:
Rate control: The ventricular rate should be adequately
controlled in all patients with AF.
Rhythm control: AF should be converted to normal si-
nus rhythm with electrical cardioversion or pharmaco-
logic therapy in selected patients with AF.
Prevention of thromboembolism: Anticoagulation is
one of the cornerstones in the therapy of AF. It should be
considered in all patients who are high risk for stroke.
Rate Control
The ventricular rate should always be adequately controlled
in all patients with AF. ABCD are the drugs of choice for
controlling the ventricular rate in AF as well as in atrial
flutter (Amiodarone, Beta blockers, Calcium channel
blockers, Digoxin). The drugs of choice are not necessarily
LWBK271-C19_246-261.qxd 1/29/09 12:57 PM Page 255 LWBK271-C01_01-08.qxd
in alphabetical order. Beta blockers, nondihydropyridine
calcium channel blockers, and digoxin are effective for rate
control. They are not effective in converting AF to normal si-
nus rhythm. They should not be given when there is preexci-
tation. Amiodarone is effective both for rate control and for
rhythm control (conversion of AF to normal sinus rhythm)
but has several side effects and is not approved by the Food
and Drug Administration for rate control or for rhythm con-
trol in AF. This agent nevertheless is included as a therapeutic
agent based on recommended guidelines and clinical efficacy
reported in the literature.
The choice of the most appropriate agent for controlling the
ventricular rate in AF in the acute setting depends on the
clinical presentation.
Normal systolic function: In stable patients with normal
systolic function, intravenous nondihydropyridine calcium
channel blockers and beta blockers receive Class I recom-
mendation for control of ventricular rate in AF. Intravenous
digoxin or amiodarone also receive Class I recommendation
when there is LV dysfunction and heart failure or when the
use of other AV nodal blocking agents are inappropriate.
n Nondihydropyridine calcium channel blockers:
n Diltiazem: Diltiazem is a nondihydropyridine cal-
cium channel blocker. The initial dose is 0.25 mg/kg
(or 15 to 20 mg) given IV over 2 minutes. The heart
rate and blood pressure should be monitored care-
fully. The drug has a rapid onset of action and should
control the ventricular rate within 5 to 10 minutes of
administration. If the heart rate remains tachycardic
10 minutes after the initial bolus, a higher dose of
0.35 mg/kg (or 20 to 25 mg) is given IV similar to the
first dose. The second dose may be more hypotensive
than the initial dose and should be given more slowly.
This will allow the blood pressure and heart rate to be
monitored more carefully while the drug is being ad-
ministered. When the heart rate is controlled, usually
below 100 bpm, a maintenance dose of 5 to 15
mg/hour (usually 10 mg/hr) is infused. Diltiazem has
a short half life of 3 to 4 hours, but becomes more
prolonged when maintenance infusion is added. The
IV maintenance dose is titrated according to the de-
sired heart rate. An oral maintenance dose of dilti-
azem is started within 3 hours after the initial IV dose
so that the IV infusion can be discontinued within
24 hours. The total oral dose is usually 1.5 times the
expected 24-hour cumulative IV dose. A total of 120
to 360 mg of short-acting diltiazem is given orally in
three to four divided doses. A long-acting prepara-
tion can be given once or twice daily.
n Verapamil: Verapamil is another nondihydropyri-
dine calcium channel blocker. The initial dose is
0.075 to 0.15 mg/kg (or 5 to 10 mg) given IV over
2 minutes. The same dose can be repeated after 15
to 30 minutes if needed. Verapamil has a longer
duration of action of 4 to 12 hours and, unlike
Atrial Fibrillation 255
diltiazem, does not need a continuous mainte-
nance IV infusion. It is more hypotensive and
more negatively inotropic than diltiazem; thus, the
patient should be carefully monitored especially if
the patient is already on a beta blocker. The hy-
potension may respond to calcium gluconate given
1 gram IV. Oral maintenance dose is 120 to 360 mg
daily in divided doses. A long-acting preparation
can be given once daily.
n Beta blockers: Beta blockers are preferred in patients
with myocardial ischemia or thyrotoxicosis and also
receive Class I recommendation for rate control.
n Metoprolol: Metoprolol is a selective 1 blocker.
The initial dose is 2.5 to 5 mg IV over 2 minutes up
to three doses (maximum dose of 15 mg given
within 15 minutes). This is followed by an oral
maintenance dose of 25 to 100 mg (usually 50 mg)
given twice daily. The oral dose is titrated accord-
ing to the desired heart rate.
n Atenolol: Atenolol is also a selective 1 blocker. It
does not carry indication for controlling the ven-
tricular rate of AF, but is approved for use in hy-
pertension and acute myocardial infarction. The
initial dose is 5 mg IV over 5 minutes. A second
dose may be given 10 minutes later if needed, for a
total intravenous dose of 10 mg. This is followed
by an oral dose of 50 mg 10 minutes after the last
intravenous dose and another 50 mg 12 hours
later. A maintenance oral dose of 50 mg is given
once daily. The oral dose is titrated according to
the desired heart rate.
n Propranolol: This is a nonselective 1 2 blocker.
The initial dose is 0.15 mg/kg IV. Up to 10 mg is
given slowly IV at 1 mg per minute. The IV dose is
followed by an oral dose of 80 to 240 mg daily
given in divided doses. The oral dose is titrated ac-
cording to the heart rate. A long-acting prepara-
tion is also available and is given once daily.
n Esmolol: This agent is ultrashort-acting with a
half-life of 9 minutes. A loading dose is needed,
which is 0.5 mg/kg (500 mcg/kg) infused over a
minute. This is followed by an initial maintenance
dose of 0.05 mg/kg/min (50 mcg/kg/minute) in-
fused for 4 minutes. The patient is evaluated after
5 minutes if a higher maintenance dose is needed.
The patient should be carefully monitored during
infusion so that the appropriate maintenance dose
can be adjusted, which can vary up to 60 to 200 mcg/
kg/minute. See Appendix: Commonly Used Injectable
Pharmacologic Agents for further dosing.
n Digoxin: This agent is not the preferred agent when LV
function is preserved. However, when there is hypoten-
sion (preventing the use of calcium channel blockers
or beta blockers) or the patient has bronchospastic
pulmonary disease (preventing the use of beta blockers)
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256 Chapter 19
or patient has LV dysfunction or heart failure, this
agent receives a Class I recommendation. It is not
effective as monotherapy and is generally combined
with other AV nodal blocking agents for rate control.
Dosing is described under LV dysfunction.
n Amiodarone: In patients with normal systolic func-
tion, amiodarone given intravenously receives a Class
IIa recommendation for rate control when other AV
nodal blocking agents are ineffective or inappropriate.
It receives a Class IIb recommendation when given
orally to control heart rate when other agents have
been tried and are unsuccessful in controlling the ven-
tricular rate at rest or during exercise. Dosing is de-
scribed under LV dysfunction.
Patients with LV systolic dysfunction: In patients with
heart failure, digoxin and amiodarone are the preferred
agents.
n Digoxin: Digoxin receives a Class I recommendation
when given orally or intravenously when there is heart
failure from LV systolic dysfunction. A loading dose is
necessary and may vary. For rapid control of ventricular
rate in the acute setting, the initial dose recommended
by the ACC/AHA/ESC 2006 guidelines on the manage-
ment of AF is 0.25 mg IV over 2 minutes every 2 hours.
The dose should not exceed 1.5 mg IV within 24 hours.
Maintenance dose is 0.125 to 0.375 mg daily given in-
travenously or orally. For heart rate control in a non-
acute setting, an oral dose of 0.5 mg daily may be given
for 2 to 4 days followed by an oral maintenance dose of
0.125 to 0.375 mg daily. Digoxin has a very slow onset of
action (1 hour or more) and its maximal effect is not
until after 6 hours. It is usually not a very effective agent
in controlling the ventricular rate in AF when used as
monotherapy and receives a Class III recommendation
when given as the sole agent in patients with paroxys-
mal AF. It may be effective in controlling heart rates at
rest as well as in individuals who are sedentary but con-
trol of the rate of atrial fibrillation is lost during physi-
cal activity or in conditions associated with adrenergic
stress such as febrile illnesses, hyperthyroidism, or exac-
erbations of chronic obstructive pulmonary disease.
n Amiodarone: Intravenous amiodarone receives a
Class I recommendation to control the ventricular
rate in patients with AF with heart failure. In the acute
setting when rate control is necessary, 150 mg is given
IV over 10 minutes followed by a maintenance infu-
sion of 1 mg/minute IV for 6 hours and 0.5
mg/minute IV for the next 18 hours. The oral dose has
a very slow onset of action and is more appropriate to
use in nonacute setting. The oral dose is 800 mg daily
in divided doses for 1 week. Another option is to give
a lower dose of 600 mg daily in divided doses for 1
week or 400 mg daily in divided doses for 4 to 6 weeks.
Any of these regimens is followed by long-term oral
maintenance dose of 200 mg daily. Amiodarone affects
the pharmacokinetics of warfarin, verapamil, and
digoxin. The dose of these pharmacologic agents
should be reduced when amiodarone is started.
n Other agents: Intravenous injection of nondihydropy-
ridine calcium channel blockers and beta blockers may
be given cautiously for rate control when there is LV
dysfunction. These agents however are contraindicated
(Class III) when the patient is acutely decompensated.
Diltiazem has a shorter half-life and is less negatively
inotropic than verapamil and may be more tolerable.
WPW syndrome: In patients with WPW syndrome, the
use of AV nodal blocking agents to control ventricular
rate during AF is inappropriate and may be dangerous.
Inhibition of the AV node with any AV nodal blocking
agents such as calcium channel blockers, beta blockers, or
digitalis will allow atrial fibrillatory impulses to pass more
efficiently through the bypass tract, which may result in
ventricular fibrillation. Instead of AV nodal blockers, an-
tiarrhythmic agents that increase the refractory period of
the bypass tract such as type IA agents (procainamide) or
drugs that can inhibit both AV node and bypass tract such
as type IC and type III agents (ibutilide or amiodarone),
may be given intravenously to hemodynamically stable
patients to control the ventricular rate. Otherwise, the AF
should be converted to normal sinus with electrical car-
dioversion. The treatment of AF in patients with WPW
syndrome is further discussed in Chapter 20, Wolff-
Parkinson-White Syndrome.
Nonpharmacologic control of ventricular rate in AF:
The following are used only when pharmacologic agents are
not effective in controlling the ventricular rate, especially
when there is tachycardia-mediated cardiomyopathy.
AV nodal ablation: If the ventricular rate in AF can not
be controlled with AV nodal blocking agents or other an-
tiarrhythmic agents, radiofrequency ablation of the AV
node combined with insertion of a permanent ventricular
pacemaker is an option. Before AV nodal ablation is con-
sidered, the patient should be tried on medications and
performed as a last resort especially in patients with
tachycardia-mediated cardiomyopathy.
Pulmonary vein isolation: Isolation of the pulmonary
veins may be performed either surgically or with radio-
frequency ablation to maintain normal sinus rhythm (see
Rhythm Control in this chapter) rather that for control of
ventricular rate during AF.
Rate control: The following is a summary of pharmacologic
agents recommended by the ACC/AHA/ESC guidelines for
rate control in AF (Table 19.1).
Rhythm Control
Rhythm control or conversion of AF to normal sinus rhythm
is not necessary in all patients with AF. In the AFFIRM (Atrial
Fibrillation Follow-up Investigation of Rhythm Manage-
ment) and RACE (Rate Control vs. Electrical Cardioversion
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TABLE 19.1
Doses of Pharmacologic Agents for Rate
Control in AF
Pharmacologic
Agents Initial and Maintenance Doses
Diltiazem 0.25 mg/kg IV over 2 min followed by
IV maintenance dose of 515 mg/hr
Verapamil 0.0750.15 mg/kg IV over 2 min
Metoprolol 2.55.0 mg IV over 2 min up to 3 doses
Propranolol 0.15 mg/kg IV
Esmolol 500 mcg/kg IV over 1 min loading dose;
maintenance dose is 60200 mcg/kg/
min IV
Digoxin 0.25 mg IV each 2 hr up to 1.5 mg and
maintenance dose is 0.125 to
0.375 mg daily IV or orally
Amiodarone 150 mg over 10 min IV loading dose
and maintenance dose of 0.5 to
1.0 mg/min IV
The table summarizes the doses of pharmacologic agents recom-
mended by the American College of Cardiology/American Heart
Association/European Society of Cardiology 2006 practice guide-
lines for control of ventricular rate in AF. Any of these agents may be
given to patients with normal systolic function although in patients
with left ventricular dysfunction, especially in patients with acute
decompensated heart failure, only digoxin or amiodarone are the
preferred agents.
AF, atrial fibrillation; IV, intravenous.
for Persistent Atrial Fibrillation) trials, there was no differ-
ence in mortality or incidence of stroke among patients with
AF who were treated aggressively with electrical cardiover-
sion and maintenance of the AF to normal sinus rhythm with
antiarrhythmic agents when compared with patients with AF
who were not cardioverted and were given only AV nodal
blocking agents to control the ventricular rate. Both groups
were anticoagulated. Thus, rhythm control in patients with
AF should be individualized and should be reserved for pa-
tients who are symptomatic because quality of life can be im-
proved, especially among patients with low cardiac output
from LV dysfunction.
Methods of converting AF to normal sinus rhythm:
Rhythm control or conversion of AF to normal sinus rhythm
can be achieved with pharmacologic therapy or electrical
cardioversion. Conversion of AF to normal sinus rhythm
carries the risk of thromboembolization whether the conver-
sion is spontaneous, electrical, or pharmacologic. The risk is
increased if the duration of the AF is 48 hours. The longer
the duration of AF, the higher the risk of thromboemboliza-
tion because the atria will remain paralyzed even after the
rhythm has converted to normal sinus. This risk is highest
immediately after cardioversion, when AF has converted to
normal sinus rhythm. Even among patients with negative
transesophageal echocardiogram, atrial thrombi may develop
Atrial Fibrillation 257
after cardioversion from atrial stunning resulting in stagnant
flow in the atria and left atrial appendage.
Spontaneous conversion: Spontaneous conversion of
AF to normal sinus rhythm can occur in a large number of
patients with acute onset AF. Spontaneous conversion oc-
curs most frequently during the first 24 to 48 hours. The
chance of spontaneous conversion to normal sinus rhythm
becomes less and less as the duration of AF becomes longer.
The chance of spontaneous conversion is significantly less
when the duration of AF is more than 7 days. Additionally,
the efficacy of antiarrhythmic agents in converting AF to
normal sinus rhythm also becomes markedly diminished if
the patient is in AF for more than 7 days.
Pharmacologic therapy: The use of drugs to convert
patients with AF to normal sinus rhythm is simpler when
compared with electrical cardioversion because it does
not require IV sedation. They are most effective when
given within 7 days of AF onset. Pharmacologic car-
dioversion however is less effective than electrical car-
dioversion. The toxic effect of these agents is also a major
issue since most of these agents are proarrhythmic.
Among the pharmacologic agents that have been shown
to be effective in converting AF to normal sinus rhythm
are type IA agents (procainamide, quinidine, and disopy-
ramide), type IC agents (propafenone and flecainide),
and type III agents (ibutilide, dofetilide, and amio-
darone). When any of these agents are given to convert AF
to normal sinus rhythm, the patient should be hospital-
ized. The only exception is amiodarone, which is the least
proarrhythmic and can be initiated orally in the outpa-
tient setting. Types IA and IC agents can potentially cause
AF to convert to atrial flutter with one to one conduction
across the AV node. An AV nodal blocker such as a beta
blocker or a nondihydropyridine calcium channel blocker
therefore should be given at least 30 minutes before these
agents are administered. The pharmacologic agent of
choice to terminate AF to normal sinus rhythm will de-
pend on the duration of the AF as well as the presence or
absence of LV systolic dysfunction.
n AF of 7 days duration: According to the ACC/AHA/
ESC 2006 guidelines for the management of patients
with AF, the following agents have been proven effec-
tive for pharmacological conversion of AF to normal
sinus rhythm when the AF is 7 days duration. These
agents can be given orally or intravenously. Agents
that are most effective include Class IC agents (fle-
cainide or propafenone) and Class III agents (dofetilide
or ibutilide). These agents carry a Class I recommen-
dation for pharmacologic conversion of AF to normal
sinus rhythm. Less effective is amiodarone, which car-
ries a Class IIa recommendation. Other antiarrhyth-
mic agents such as Class IA agents (quinidine, pro-
cainamide, and disopyramide) are less effective and
carry a Class IIb recommendation. The use of sotalol
and digoxin is not recommended and should not be
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258 Chapter 19
administered for conversion of AF to normal sinus
rhythm (Class III recommendation).
Preserved systolic function: There are several agents
that can be used to convert AF to normal sinus rhythm
when LV systolic function is preserved.
Flecainide: This agent receives Class I recommendation
and can be given orally or intravenously. The oral dose for
flecainide is 200 to 300 mg given once. The oral dose
should not be given out of hospital for the patient to self
administer as a pill in the pocket strategy unless the
drug has been tried and proven to be safe and effective
during initial hospitalization. An AV nodal blocker such
as a calcium channel blocker or a beta blocker should be
given at least 30 minutes before flecainide is given to pre-
vent rapid ventricular rates from occurring should the
rhythm convert to atrial flutter. The IV dose is 1.5 to 3.0
mg/kg given over 10 to 20 minutes. The intravenous
preparation is not available in the United States.
Propafenone: The drug also receives a Class I recom-
mendation and can be given orally or intravenously. The
oral dose is 600 mg given once. The IV dose is 1.5 to 2.0
mg/kg given over 10 to 20 minutes. The intravenous
preparation is not available in the United States. The suc-
cess rate varies from 56% to 83%. Similar to flecainide,
the agent can be prescribed for self-administration by the
patient as a pill in the pocket strategy only after initial
therapy in the hospital has shown that the drug is safe and
effective and the patient does not have any evidence of
sick sinus syndrome or structural cardiac disease. AV
nodal blockers are routinely given as background therapy
in AF. Otherwise, if the patient is not on AV nodal blocker,
it should be given at least 30 minutes before taking a type
IC agent to prevent one to one conduction across the AV
node should the patient develop atrial flutter.
Ibutilide: The drug is available only intravenously and
receives a Class I recommendation. The drug is given over
10 minutes as a 1 mg dose, diluted or undiluted. The dose
is repeated after 10 minutes if the rhythm has not con-
verted.
Dofetilide: The drug is given only orally and receives a
Class I recommendation. Its use is restricted to cardiolo-
gists who are allowed access to this agent. Initial dosing is
based on kidney function and is contraindicated in pa-
tients with severe renal dysfunction (creatinine clearance
of 20 mL/minute). In patients with normal renal func-
tion (creatinine clearance 60 mL/minute), the dose is
500 mcg twice daily. Maintenance dose is 500 to 1,000
mcg daily. The QT interval should be carefully monitored
during therapy.
Amiodarone: The drug can be given intravenously or
orally and receives a Class IIa recommendation. The IV
dose is 5 to 7 mg/kg over 30 to 60 minutes followed by 1.2
to 1.8 g per day of continuous infusion or in divided oral
doses until a total dose of 10 g is given. The maintenance
dose is 200 to 400 mg per day. The oral dose is given only
if immediate conversion of AF to normal sinus rhythm is
not essential. The oral in-hospital dose is 1.2 to 1.8 g/day
in divided doses until 10 g is given. Maintenance dose is
200 is 400 mg/day. Another option is to give 30 mg/kg as
single dose. Amiodarone is the only antiarrhythmic agent
that can be initiated without hospitalizing the patient. In
outpatients, a smaller dose of 600 to 800 mg is given orally
daily in divided doses until a total of 10 g is given. This is
followed by a lower maintenance dose of 200 to 400 mg a
day. Amiodarone enhances the effect of warfarin and
digoxin. The doses of both agents should be reduced
when amiodarone is initiated.
Quinidine: Quinidine is given only orally and receives a
Class IIb recommendation. The dose is 0.75 to 1.5 g in di-
vided doses over 6 to 12 hours. The drug is combined
with an AV nodal blocker to prevent increase in ventricu-
lar rate before AF converts to normal sinus. The drug can
prolong the QT interval and can cause torsades de
pointes. If patient is on digoxin, serum levels should be
carefully monitored because quinidine increases the levels
of digoxin, which can result in digitalis toxicity.
Left ventricular (LV) dysfunction: When LV dysfunc-
tion (LV ejection fraction 40%) or congestive heart fail-
ure is present, only amiodarone and dofetilide (both type
III agents) are the preferred agents for conversion of AF to
normal sinus rhythm. These are the least negatively in-
otropic antiarrhythmic agents.
Amiodarone: Loading dose is described above. The
maintenance dose is 100 to 400 mg daily.
Dofetilide: The drug is given orally and its use is re-
stricted to cardiologists who are familiar with the use of
this agent. Dosing is described previously.
AF of more than 7 days duration: When AF is more
than 7 days duration, only Class III agents (amiodarone,
ibutilide, and dofetilide) are effective and are the only an-
tiarrhythmic agents recommended. Most patients with
AF of more than 7 days duration have persistent AF.
Class IA and Class IC agents are less effective and carry
a Class IIb recommendation. According to the ACC/
AHA/ESC 2006 guidelines for the management of pa-
tients with AF, sotalol and digoxin may be harmful and
are not recommended for pharmacologic conversion of
AF to normal sinus rhythm regardless of the duration of AF.
Rhythm control: The following is a summary of pharmaco-
logic agents for rhythm control according to the ACC/AHA/
ESC practice guidelines for management of patients with AF
(Table 19.2).
Electrical or direct current cardioversion: This proce-
dure is performed under intravenous sedation. If the AF
is more than 48 hours duration, DC cardioversion
should not be performed until after the patient is ade-
quately anticoagulated for a minimum of 3 weeks. If the
need for conversion to normal sinus rhythm is more im-
mediate, electrical cardioversion can be carried out if a
transesophageal echocardiogram can be performed and
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Atrial Fibrillation 259

TABLE 19.2

Pharmacologic Agents for Conversion of AF to Normal Sinus Rhythm

Pharmacologic Agents Recommended Doses
Amiodarone Oral: 1.21.8 g daily in divided doses until 10 g total
(Class III agent) then maintain dose to 200400 mg daily or 30 mg/kg
as a single dose
IV/oral: 57 mg/kg over 3060 min IV, then 1.21.8 g
daily continuous IV or orally in divided doses until a
total of 10 g, then 200400 mg daily
Dofetilide (Class III) Oral only: Normal kidney function (creatinine clearance
60 mL/min, 500 mcg BID. The dose is adjusted in
patients with renal dysfunction
Ibutilide (Class III) IV only: 1 mg over 10 min. Repeat after 10 min with the
same dose if necessary
Flecainide (Class IC) Oral: 200300 mg one dose
IV: 1.5 to 3.0 mg/kg over 1020 min (the IV dose is not
available in the United States)
Propafenone (Class IC) Oral: 600 mg one dose
IV: 1.5 to 2.0 mg/kg over 1020 min (the IV dose is not
available in the United States)
Quinidine (Class IA) Oral only: 0.75 to 1.5 g in divided doses over 612 h usually
with another agent that will slow ventricular rate
The table summarizes the doses of pharmacologic agents recommended by the American College of
Cardiology/American Heart Association/European Society of Cardiology practice guidelines for con-
version of AF to normal sinus rhythm. In patients with left ventricular dysfunction, only amiodarone
and dofetilide are the preferred agents.
AF, atrial fibrillation; IV, intravenous.

no evidence of intracardiac thrombi can be demon-
strated.
n Electrical cardioversion is the most effective in con-
verting AF to normal sinus rhythm. Most patients will
need an initial energy setting of 200 joules for conver-
sion. The energy setting is increased gradually if the
initial shock is unsuccessful. The shock is synchronized
with the QRS complex to prevent the delivery of the
shock during the vulnerable phase of the cardiac cycle,
which can result in ventricular fibrillation. Devices
Prevention of Stroke
that deliver direct current cardioversion with biphasic
waveform have been shown to be more effective than
devices that deliver the monophasic waveform.
n The patient should be adequately anticoagulated and
should preferably be on antiarrhythmic agent before
electrical cardioversion is performed.
Nonpharmacologic therapy: This is another option in
converting patients with AF especially in symptomatic
patients with recurrent AF who are not responsive to
medical therapy.
n Surgical ablation: Maze procedure is performed by
making atrial incisions at certain critical geographic
location in the atria so that AF will not become sus-
tained. This is usually performed in patients with AF
in conjunction with other cardiac surgical procedures
such as replacement or repair of mitral valve or during
coronary bypass surgery.
n Catheter ablation: This procedure involves isolation
of the pulmonary veins similar to a surgical maze pro-
cedure but is performed with catheterization tech-
niques. The pulmonary veins are usually the site of
ectopic foci that can precipitate AF.
AF is a common cause of stroke in the elderly. The use of an-
tithrombotic agents therefore is one of the cornerstones in the
therapy of AF and is the standard of care in preventing strokes
in patients with AF. Patients with AF who are high risk for stroke
should be identified so that they can be protected with adequate
anticoagulation. This is regardless whether the AF is paroxys-
mal, persistent, or permanent. Similarly, patients with AF who
are low risk for stroke should also be identified so that they do
not have to be exposed to the side effects of anticoagulation.
Highest risk of stroke: Patients with AF who are highest
risk of stroke (6% per year) needs to be fully anticoagu-
lated with warfarin. The following patients with AF are
highest risk for stroke:
n Valvular AF: Patients with valvular AF are very high
risk for developing stroke. Valvular AF includes patients
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260 Chapter 19
with rheumatic mitral stenosis as well as patients with
prosthetic mitral valve or previous mitral valve repair.
Their risk for thromboembolism is approximately 15
to 20 times that of patients with AF but without these
cardiac abnormalities. Patients with mitral prosthetic
valves should be anticoagulated with warfarin to an
International Normalized Ratio (INR) of 2.5 to 3.5.
Patients with mitral stenosis and previous mitral valve
repair should be anticoagulated to an INR of 2.0 to 3.0.
n Previous history of thromboembolism: Patients with
AF with previous history of stroke, transient ischemic
accident (TIA), or other forms of thromboembolism
are also at high risk for developing stroke. Their risk is
increased 2.5 times those with AF but without previ-
ous history of thromboembolism. These patients
should also be anticoagulated with warfarin to an INR
of 2.0 to 3.0.
Lowest risk of stroke: Patients with AF who are lowest
risk for stroke ( 2% per year) are patients with lone AF.
The ACC/AHA/ESC 2006 guidelines on AF defines lone
AF as patients who are 60 years of age and have no evi-
dence of cardiac or pulmonary disease. These patients are
not hypertensive and have normal echocardiograms and
are low risk for thromboembolism. The guidelines rec-
ommend that these patients should be on aspirin, 81 to
325 mg daily although they also have the option of receiv-
ing no therapy. Among patients 60 years of age with
heart disease but none of the risk features for throm-
boembolism, these patients are also low risk for stroke but
should be on aspirin 81 to 325 mg daily. These patients do
not need to be anticoagulated with warfarin.
Intermediate or moderate risk for stroke: Some pa-
tients with nonvalvular AF (no prosthetic mitral valve or
rheumatic mitral stenosis) may have risk features for
stroke that are intermediate (3% to 5% per year) when
compared with patients in AF, but without these risk fea-
tures. These intermediate risk markers come under the
eponym of CHADS2.
n C  Cardiac failure or left ventricular dysfunction
(ejection fraction 35%)
n H  Hypertension
n A  Advanced age (75 years)
n D  Diabetes mellitus
n S2  Stroke, TIA, or previous history of thromboem-
bolism.
n In nonvalvular AF, each of the above risk features
increases the incidence of stroke and receives a
weight of one except stroke/TIA or previous his-
tory of thromboembolism, which gives the patient
two times the risk of the other risk features and is
thus equivalent to a weight of 2, thus S2.
n CHADS2 serves as a useful guide in determining
the intensity of antithrombotic therapy in patients
with nonvalvular AF.
One intermediate risk feature: Any one of the above
risk features: cardiac failure, hypertension, advanced age,
and diabetes (CHAD) but not stroke or TIA, is an inter-
mediate risk for thromboembolism. These patients have
the option of either taking aspirin 81 to 325 mg daily or
warfarin monitored to an INR of 2 to 3.
Previous history of stroke or two or more risk fac-
tors: Patients with history of stroke or TIA or with 2 or
more intermediate risk features should receive warfarin
and should be anticoagulated to an INR of 2.0 to 3.0.
Anticoagulation during electrical or pharmacologic
cardioversion: If cardioversion is planned in patients with
AF of more than 48 hours duration or the duration of AF is
not known, these patients should be anticoagulated for at
least 3 to 4 weeks before electrical or pharmacologic car-
dioversion is attempted. If immediate cardioversion is
planned, the patient should undergo transesophageal
echocardiography to exclude thrombus in the left atrial ap-
pendage. If a thrombus is present, cardioversion is delayed
and the patient is fully anticoagulated for at least 3 to 4 weeks
before electrical cardioversion can be performed. If a throm-
bus is not present, intravenous heparin is given and electrical
cardioversion is performed under intravenous anesthesia.
Anticoagulation is continued after successful cardioversion
for at least 3 to 4 weeks preferably 12 weeks. This includes pa-
tients with lone AF who undergo cardioversion. In many pa-
tients who are successfully cardioverted, the normal sinus
rhythm in the ECG is often not accompanied by effective
atrial contraction. This electromechanical dissociation may
persist for several days or weeks. Thus, anticoagulation
should be continued. The risk of stroke is similar among pa-
tients undergoing pharmacologic or electrical cardioversion
and is highest within 3 days after the procedure. Among pa-
tients developing strokes after cardioversion, all episodes oc-
curred within 10 days after the procedure.
Warfarin is the standard treatment for anticoagulating pa-
tients with AF. Aspirin does not equal the protection given by
warfarin except in patients with lone AF or those with a 0 to
1 risk factor for stroke.
Table 19.3 summarizes the use of antithrombotic agents in
patients with AF.
Prognosis
AF is more common in the elderly and is an independent risk
factor for death. The mortality in patients with AF is twice
that of patients in normal sinus rhythm. This increase in
mortality is associated with the severity of the underlying
heart disease.
AF is associated with increased risk of stroke and heart fail-
ure. It is a common cause of morbidity in elderly patients
with approximately 15% of all thromboembolic strokes from
AF.
In patients younger than 60 years of age without clinical or
echocardiographic evidence of structural heart disease or
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Atrial Fibrillation 261

TABLE 19.3

Antithrombotic Agents for Prevention of Stroke in AF

Low Risk Moderate Risk High Risk
Lone atrial fibrilla- Any one of the follow- Valvular AF or previous
tion ing intermediate risk history of stroke or tran-
features: sient ischemic attack or 2
Aspirin Congestive heart failure or more intermediate risk
81325 mg daily or ejection fraction features
or no therapy 35%, hypertension, age
75 years or diabetes Warfarin (INR of 2.03.0)
Age 60 years, has
heart disease but For mechanical mitral
no risk features Aspirin 81325 mg daily valve
or
Aspirin Warfarin (INR 2.03.0) Warfarin (INR 2.5.5)
81325 mg daily
The table summarizes the antithrombotic agents recommended by the 2006 American College of
Cardiology/American Heart Association/European Society of Cardiology guidelines for prevention of
stroke in patients with AF.
AF, atrial fibrillation; IV, intravenous; INR, International Normalized Ratio.

chronic pulmonary disease, AF is generally benign. The risk
of stroke, however, increases above this age or when associ-
ated with conditions that are known to increase the risk for
stroke.
Suggested Readings
The Atrial Fibrillation Follow-up Investigation of Rhythm Man-
agement (AFFIRM) Investigators. A comparison of rate con-
trol and rhythm control in patients with atrial fibrillation.
N Engl J Med. 2002;347:18251833.
Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
ACC/AHA/ESC Guidelines for the management of pa-
tients with supraventricular arrhythmiasexecutive sum-
mary. A report of the American College of Cardiology/
American Heart Association Task Force on Practice Guide-
lines, and the European Society of Cardiology Committee
for Practice Guidelines (Writing Committee to Develop
Guidelines for the Management of Patients with Supraven-
tricular Arrhythmias). J Am Coll Cardiol. 2003;42:
14931531.
Botteron GW, Smith JM. Cardiac arrhythmias. In: Carey CF, Lee
HH, Woeltje KF, eds. The Washington Manual of Medical
Therapeutics. 29th ed. Philadelphia: Lippincott Williams &
Wilkins; 1998:130156.
Capucci A, Villani GQ, Piepoli MF. Reproducible efficacy of
loading oral propafenone in restoring sinus rhythm in pa-
tients with paroxysmal atrial fibrillation. Am J Cardiol. 2003;
92:13451347.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006
guidelines for the management of patients with atrial fibril-
lationexecutive summary; a report of the American Col-
lege of Cardiology/American Heart Association Task Force
and the European Society of Cardiology Committee on Prac-
tice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (Writing Committee to
Revise the 2001 Guidelines for the Management of Patients
with Atrial Fibrillation). J Am Coll Cardiol. 2006;48:854906.
Gage BF, Waterman AD, Shannon W, et al. Validation of clinical
classification schemes for predicting stroke: results from the
National Registry of Atrial Fibrillation. JAMA. 2001;285:
28642870.
Rockson SG, Albers GW. Comparing the guidelines: anticoagu-
lation therapy to optimize stroke prevention in patients with
atrial fibrillation. J Am Coll Cardiol. 2004;43:929935.
Roy D, Talajic M, Nattel S, et al. Rhythm control versus rate con-
trol for atrial fibrillation and heart failure. N Engl J Med.
2008;358:26672677.
Sherman DG, Kim SG, Boop BS, et al. Occurrence and charac-
teristics of stroke events in the atrial fibrillation follow-up
investigation of sinus rhythm management (AFFIRM) study.
Arch Intern Med. 2005;165;11851198.
Singh BN, Singh SN, Reda DJ, et al. Amiodarone versus sotalol
for atrial fibrillation. N Engl J Med. 2005;352:18611872.
Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate
control and rhythm control in patients with recurrent persist-
ent atrial fibrillation. N Engl J Med. 2002;92:18341840.
van Walraven WC, Hart RG, Wells GA, et al. A clinical prediction
rule to identify patients with atrial fibrillation and a low risk
for stroke while taking aspirin. Arch Intern Med. 2003;163:
936943.
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20
Wolff-Parkinson-White
Syndrome
Anatomy of the Conduction System
Wolff-Parkinson-White (WPW) syndrome: WPW
syndrome is a clinical entity characterized by preexcita-
tion of the ventricles with symptoms of paroxysmal
tachycardia.
Preexcitation of the Ventricles
Normal atrioventricular (AV) conduction: In nor-
mal individuals, the atria and ventricles are separated
by a dense mass of fibrous tissues that prevent the
spread of electrical impulses from atria to ventricles.
The only pathway by which the atrial impulse can
reach the ventricles is through the AV node and nor-
mal intraventricular conduction system (Fig. 20.1A).
WPW syndrome: In WPW syndrome, a bypass
tract is present, which connects the atrium directly
to the ventricle. The atrial impulse therefore is able
to reach the ventricles not only through the AV
node, but also through the bypass tract (Fig. 20.1B).
This accessory pathway can cause premature activa-
tion of the ventricles. It can also serve as a pathway
for reentry, which may result in clinical symptoms
of paroxysmal tachycardia.
Ventricular preexcitation: When a bypass tract is
present, conduction of the sinus impulse to the ventri-
cles is altered as shown in Figure 20.2.
Atrial activation: During normal sinus rhythm, ac-
tivation of the atria is not altered. The sinus P wave
remains normal.
Ventricular activation: When a bypass tract is
present, the ventricles are activated through two
separate pathways: the AV node and bypass tract.
The QRS complex represents a fusion complex.

Sinus
Node

Atria Atria

AV Node Fibrous Bypass

Tissues tract

AV Node

Ventricles Ventricles

A. Normal AV Conduction B. WPW Syndrome

The Conduction System in Normal Individuals and in Patients with

Figure 20.1:
the WPW Syndrome. (A) The normal AV conduction system. The atrial impulse can enter
the ventricles only through the AV node (arrow). (B) A bypass tract connecting the atrium
directly to the ventricle across the AV groove. When a bypass tract is present, an atrial impulse
can enter the ventricles not only through the AV node but also through the bypass tract
(arrows). AV, atrioventricular.

262
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Wolff-Parkinson-White Syndrome 263

Atria
Atria Atria

Bypass AV Impulse is
tract Node delayed at
the AV
Ventricles
node
Ventricles Ventricle is Ventricles
activated
prematurely
A B C
Delta wave Delta wave

Figure 20.2: Ventricular Preexcitation. (A) The sinus impulse activates the atria and a P wave
is normally recorded. (B) The sinus impulse is normally delayed at the AV node but is conducted
directly through the bypass tract causing the ventricles to be prematurely activated. This causes the
PR interval to shorten and the initial portion of the QRS complex to be slurred. (C) The impulse
finally emerges from the atrioventricular node and activates the rest of the ventricles normally.

n Bypass tract: Unlike in normal individuals in
whom the sinus impulse can reach the ventricles
only through the AV node, the presence of a bypass
tract allows the atrial impulse to be conducted di-
rectly to the ventricles thus activating the ventricles
prematurely. This causes the PR interval to be
shorter than normal (Fig. 20.2B). The impulse
spreads by muscle cell to muscle cell conduction
causing the initial portion of the QRS complex to
be inscribed slowly. This slow initial upstroke of
the QRS complex is called the delta wave.
n AV node: The sinus impulse is normally delayed
at the AV node. As the impulse emerges from
The Bypass Tract
the AV node, it activates the ventricles rapidly
through the normal conduction system causing the
rest of the QRS complex to be inscribed normally
(Fig. 20.2C).
Electrocardiogram Findings
Electrocardiogram (ECG) findings: The classical
ECG findings in WPW syndrome include a short PR
interval, a delta wave, and secondary ST and T wave ab-
normalities.
Short PR interval: The PR interval is short since
the bypass tract conducts more rapidly than the AV
node causing the ventricles to be excited prema-
turely. The PR interval is shorter than normal, but
does not have to measure 0.12 seconds.
Delta wave: The delta wave is the initial portion of
the QRS complex with a slow upstroke, as shown in
Figure 20.3. It represents premature activation of
the ventricles at the area of insertion of the bypass
tract. Because conduction of the impulse is by direct
muscle spread, which is slow and inefficient, this
causes the initial portion of the QRS complex to be
inscribed sluggishly. This initial portion with the
slurred upstroke is called the delta wave.
ST and T wave abnormalities: The ST and T wave
changes are secondary to the abnormal activation of
the ventricles. The direction of the ST segment and
T wave is opposite that of the delta wave.
Bypass tract: Unlike the His-Purkinje system, the by-
pass tract consists of ordinary heart muscle and does
not contain cells that are specialized for conduction.
The bypass tract may be left sided or right sided.
It may be single or multiple.
Conduction may be constant or intermittent (Figs.
20.4 and 20.5).
The bypass tracts may be active or inactive.
The bypass tract may conduct only anterogradely
(from atrium to ventricle), only retrogradely (from
ventricle to atrium) or both.
n Manifest or overt bypass tract: The bypass tract
is manifest or overt if it is capable of conducting
anterogradely from atrium to ventricle resulting
in the classical pattern of preexcitation.
n Concealed bypass tract: The bypass tract is con-
cealed if it is capable of conducting only retro-
gradely from ventricle to atrium. The baseline
ECG will not show any evidence of preexcitation
during normal sinus rhythm, but the presence of
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264 Chapter 20

Delta wave

Short PR Interval

ST and T wave
abnormalities

Figure 20.3: Ventricular Preexcitation. A QRS complex is magnified from the rhythm strip to show the short
PR interval measuring 0.11 seconds, delta wave, and ST-T abnormalities.

Normal Conduction Preexcitation

V1

Figure 20.4: Intermittent Preexcitation. The rhythm strip is recorded in V1. The first three
complexes show no evidence of preexcitation. The PR interval is prolonged and the QRS
complexes are narrow. The last three complexes show ventricular preexcitation. The PR interval
is short, the QRS complexes are wide and delta waves are present.The ST segments are also de-
pressed with inverted T waves pointing away from the direction of the delta wave.

#1 #2 #3 #4

Figure 20.5: Intermittent Preexcitation. Intermittent preexcitation is shown by arrows #1#4. The other
complexes are conducted normally without preexcitation.
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Wolff-Parkinson-White Syndrome 265

Atria
Atria

Left sided Right sided

AV bypass bypass
Node tract is tract is
farther closer to
from sinus sinus node
Ventricles node Ventricles

A B

The delta wave is barely The delta wave is very

recognizable (arrows) prominent (arrows)

Figure 20.6: Size of the Delta Wave. (A) The delta wave is barely recognizable because of a
smaller amount of myocardium activated from the bypass tract. This occurs when the bypass tract is left
sided or conduction through the AV node is enhanced. (B) The delta wave is more prominent because a
larger amount of myocardium is activated from the bypass tract. This is often seen in right sided bypass
tracts or when there is delay in the conduction of the impulse at the AV node. AV, atrioventricular.

a bypass tract can potentially cause a reentrant

tachycardia to occur. Localizing the Bypass Tract

An ECG is helpful in predicting the location of the bypass

The Delta Wave
Size of the delta wave: The delta wave may be very
conspicuous or it may be barely recognizable in the
baseline ECG, depending on the amount of ventricular
myocardium activated from the bypass tract.
Small delta wave: The delta wave may be barely rec-
ognizable if only a small amount of ventricular my-
ocardium is activated from the bypass tract. This oc-
curs if the bypass tract is left sided because a left-sided
bypass tract is farther from the sinus node compared
with a right-sided bypass tract. The farther the dis-
tance from the sinus node, the longer it takes for the si-
nus impulse to reach the bypass tract (Fig. 20.6A). This
may result in normal or near normal PR interval. The
delta wave is also small and inconspicuous if the atrial
impulse is efficiently conducted through the AV node.
Large or prominent delta wave: The delta wave is
prominent if a larger portion of the myocardium is
activated from the bypass tract (Fig. 20.6B). This oc-
curs when the bypass tract is right sided bringing it
closer to the sinus node. The delta wave is also promi-
nent if the sinus impulse is delayed at the AV node.
tract during normal sinus rhythm, during narrow com-
plex tachycardia, and during wide complex tachycardia.
After preexcitation is diagnosed in the 12-lead ECG,
the bypass tract can be localized during sinus rhythm
by the following observations.
Left-sided bypass tract: When the bypass tract is
left sided, the left ventricle is activated earlier than
the right ventricle. The impulse will travel from left
ventricle to right ventricle in the direction of V1,
which is located on the right side of the sternum
(Fig. 20.7). Thus, during normal sinus rhythm, a
positive delta wave or tall R or Rs complex will be
recorded in V1. This pattern of preexcitation is also
called type A. Tall R waves in V1 can be mistaken for
right bundle branch block, right ventricular hyper-
trophy or posterior infarction.
Right-sided bypass tract: When the bypass tract is
right sided, the right ventricle is activated earlier
than the left ventricle. The impulse spreads from
right ventricle to left ventricle away from lead V1.
This results in a negative delta wave with deep S or
rS complex in V1 (Fig. 20.8). This pattern of preex-
citation is also called type B. Because the S waves
are deeper than the R waves in V1, the ECG may be
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266 Chapter 20
Atria
V1 is located at the 4 th
intercostal space at the
right of the sternum
Ventricles
Figure 20.7: Left-Sided Bypass Tract. When the bypass tract is left sided, the initial impulse spreads from left
ventricle to right ventricle during normal sinus rhythm as shown in the above diagram (arrows). This will result in
tall R waves in V1. In this example, the bypass tract was localized at the posterior wall of the left ventricle and was
successfully ablated.
mistaken for left bundle branch block, left ventricular
hypertrophy, or anteroseptal myocardial infarction.
Location: Approximately 50% to 60% of all bypass
tracts are located at the free wall of the left ventricle,
20% to 30% at the posteroseptal area (left or right),
10% to 20% at the free wall of the right ventricle and
the remaining 5% are located in the anteroseptal area
(mostly right sided).
Left sided versus right sided: The morphology of
the QRS complex in V1 is useful in differentiating a left-
sided from a right-sided bypass tract.
Right-sided bypass tracts: As previously dis-
cussed, the bypass tract is right sided if the QRS
complex is predominantly negative (QS or rS) in V1.
Right-sided bypass tracts may be located at the pos-
teroseptal area, right ventricular free wall or an-
teroseptal area (Figs. 20.9 and 20.10).
Left-sided bypass tracts: If the QRS complex is
predominantly upright (tall R or Rs) in V1, the by-
pass tract is left sided. Left-sided bypass tracts may
be located at the left ventricular free wall or the pos-
Left Sided Bypass Tract
Left ventricle is prematurely
excited. Impulse travels in
the direction of V1.
teroseptal area. Anterior or anteroseptal bypass
tracts rarely exist because the aortic annulus and
mitral annulus are contiguous structures (Fig. 20.9).
Several methods of predicting the location of the bypass
tract during normal sinus rhythm have been described.
The bypass tract can be more accurately localized if the
delta wave contributes significantly to the QRS complex.
Although there are limitations in using the 12-lead ECG
for localizing the bypass tract, the algorithm of Olgin and
Zipes, shown below, is the simplest and most practical.
Step 1. Configuration of the QRS complex in V1:
n A tall R wave in V1 indicates that the bypass tract
is left sided.
n A deep S wave in V1 indicates that the bypass
tract is right sided.
Step 2A. Right-sided bypass tract: If the bypass
tract is right sided, it may be posteroseptal, an-
teroseptal, or free wall in location.
n Posteroseptal: QS complexes in the leads II, III,
and aVF indicate that the bypass tract is pos-
teroseptal in location.
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V1

Figure 20.8: Right-Sided Bypass Tract. When the bypass tract is right sided, the right ventricle is activated
earlier than the left ventricle. This causes the initial impulse to spread from right ventricle to left ventricle away from
lead V1 resulting in QS or rS complexes in V1. This electrocardiogram can be mistaken for left bundle branch block,
left ventricular hypertrophy, or anteroseptal myocardial infarction.

Posterior
Posteroseptal

Right
Ventricular Left
Right Free Wall TA MA Ventricular
Free Wall
Left
Ao
PA
Anteroseptal

Anterior
Figure 20.9: Location of the Bypass Tract. The position of the bypass tract at the level of
the AV grove is shown by the diagram. Right-sided bypass tracts are located at the right ventric-
ular free wall, posteroseptal, or anteroseptal areas, whereas left-sided bypass tracts are located at
the left ventricular free wall or posteroseptal area. The left anteroseptal area is occupied by the
aortic root and the presence of a left sided anteroseptal bypass tract is rare. Ao, aorta; AV,
atrioventricular; MA, mitral annulus; PA, pulmonary artery; TA, tricuspid annulus.
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268 Chapter 20

V1

Negative delta Positive delta

wave and QRS wave and QRS

Right Ventricle Left Ventricle

Isoelectric or
Negative delta
Negative delta negative delta
Left wave and QRS
wave and QRS Inferior wave in I, aVL,
axis II, III aVF
II, III, aVF axis V5, V 6

Posteroseptal Free Wall Anteroseptal Posteroseptal Free Wall

Figure 20.10: Localizing the Bypass Tract. Adapted from Olgin and Zipes.

n Anteroseptal: An inferior axis indicates that the
bypass tract is anteroseptal in location.
n Free wall: The presence of left axis indicates that
the bypass tract is located at the right ventricular
free wall.
Step 2B. Left-sided bypass tract: This may be
posteroseptal or free wall.
n Posteroseptal: QS complexes in leads II, III, and
aVF indicate that the bypass tract is posterosep-
tal in location.
n Left ventricular free wall: An isoelectric or neg-
ative delta wave in I, aVL, V5, and V6 indicates
free wall bypass tract.
R waves or Rs complexes in V1 suggest that the bypass
tract is left sided. Negative delta waves or QS complexes
in leads I and aVL suggest that the bypass tract is at the
free wall since the impulse is traveling away from these
leads.
Left-sided posteroseptal bypass tract: Example of
left-sided posteroseptal bypass tract is shown in Figure
20.12. Tall R waves are present in V1 consistent with a
left-sided bypass tract. Deep Q waves are present in II,
III, and aVF suggest that the bypass tract is posterosep-
tal because the electrical impulse is traveling away from
these leads.

Right-Sided Bypass Tract

Left-Sided Bypass Tract
Right-sided posteroseptal bypass tract: Example
Left ventricular free wall: Figure 20.11 is an example of a right-sided posteroseptal bypass tract is shown in
of a bypass tract at the free wall of the left ventricle. Tall Figure 20.13. V1 shows QS complexes consistent with a

Figure 20.11: Left Ventricular Free Wall. Tall R waves are present in V1 consistent with a left sided bypass tract.
QS complexes are present in I and aVL resembling a lateral infarct. This suggests that the impulse is traveling away
from the positive sides of leads I and aVL consistent with a bypass tract at the lateral free wall of the left ventricle.
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Wolff-Parkinson-White Syndrome 269

Figure 20.12: Left-Sided Posteroseptal Bypass Tract. Deep Q waves are present in leads II, III, and aVF re-
sembling an inferior infarct. This is consistent with a posteroseptal bypass tract. The bypass tract is left sided
because tall R waves are present in V1.

right-sided bypass tract. QS complexes are also present

in leads II, III, and aVF, suggesting that the bypass tract The WPW Syndrome
is posteroseptal in location.
Anteroseptal bypass tract: Anteroseptal bypass ECG Findings
tracts are usually right sided. Right-sided anteroseptal
bypass tract has QS or rS in V1 with the axis directed in- 1. Short PR interval
feriorly toward 30 to 120. Q wave is present in 2. Delta wave
aVL but not in V6 (Fig. 20.14). 3. ST and T wave abnormalities
Right ventricular free wall: Figure 20.15 shows a by-
pass tract at the right ventricular free wall. The QRS Mechanism
complex has a left bundle branch block pattern with
left axis deviation. QS or rS complexes are present in V1 The main abnormality in WPW syndrome is the presence of a
and the QRS complex in the frontal plane is usually di- bypass tract that is separate from the normal AV conduction
rected to the left with an axis of 30 to 60, resulting system. This anomalous pathway is also called accessory
in tall R waves in I and aVL. pathway or bundle of Kent. The bypass tract consists of

Figure 20.13: Right-Sided Posteroseptal Bypass Tract. QS complexes are present in leads II, III, and a VF
consistent with a posteroseptal bypass tract. V1 shows a QS complex consistent with a right-sided posteroseptal
bypass tract.
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270 Chapter 20

Figure 20.14: Right-Sided Anteroseptal Bypass Tract. QS complexes are present in V1 and V2 consistent
with a right sided bypass tract. The axis of the QRS complex in the frontal plane is inferior (60).This is consistent
with an anteroseptal bypass tract.

ordinary myocardium that bridges the atrium directly to the
ventricle across the AV groove.
During normal sinus rhythm, the only pathway by which the
sinus impulse can reach the ventricles is through the AV
node. The impulse is normally delayed at the AV node, re-
sulting in a PR interval of 0.12 to 0.20 seconds. If a bypass
tract is present, a second pathway is created by which the
ventricles can be activated. Thus, during normal sinus
rhythm, the impulse is normally delayed at the AV node but
is conducted directly to the ventricle through the bypass
tract. This causes the ventricle to be prematurely activated
resulting in a shorter than normal PR interval usually meas-
uring 0.12 seconds. As the impulse finally emerges from
the AV node, it is conducted rapidly through the His-Purk-
inje system allowing the rest of the ventricles to be activated
normally and more efficiently.
Preexcitation of the ventricle is seen in the ECG as a short PR
interval with a delta wave.
Shortened PR interval: The PR interval is short because
the atrial impulse reaches the ventricle faster through the
bypass tract than through the AV node. The PR interval
usually measures 0.12 seconds when there is preexcita-
tion. However, the PR interval does not always have to be
0.12 seconds for preexcitation to occur. A normal PR
interval 0.12 seconds is seen in approximately 25% of
patients with preexcitation.

Figure 20.15: Right Ventricular Free Wall. QS complexes are present in V1 consistent with a right-sided
bypass tract.There is also left axis deviation of the QRS complexes of approximately 30 consistent with a bypass
tract at the right ventricular free wall.
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Delta wave: The delta wave is the slow, slurred initial de-
flection of the QRS complex. It represents myocardial
conduction of the impulse through the ventricle at the
area of insertion of the bypass tract. The delta wave is in-
scribed sluggishly because the impulse is propagated by
direct myocardial spread. This causes the QRS complex to
be inscribed slowly and is widened.
ST-T changes: The ST and T wave abnormalities are sec-
ondary to the abnormal activation of the ventricles and
are directed away from the delta wave.
The size of the delta wave depends on the amount of my-
ocardium activated by the accessory pathway. If there is sig-
nificant delay of the impulse at the AV node, a larger portion
of myocardium will be activated through the bypass tract re-
sulting in a longer, larger, and more conspicuous delta wave.
This causes a more bizarre and wider QRS complex. If the im-
pulse is quickly and efficiently conducted across the AV node,
the amount of myocardium activated by the bypass tract will
be small and the delta wave may be barely noticeable because
most of the ventricles will be activated through the normal
His-Purkinje system. The size of the delta wave also depends
on the location of the bypass tract. A right-sided bypass tract
is closer to the sinus node than a left-sided bypass tract caus-
ing the ventricles to be activated earlier. A right-sided bypass
tract therefore is expected to have a shorter PR interval and a
more prominent delta wave than a left-sided bypass tract.
When there is preexcitation, the QRS complex is actually a
fusion complex. The initial portion of the QRS complex is
due to activation of the ventricles from the accessory path-
way. The delta wave therefore represents the impulse that is
contributed by the bypass tract. The remaining QRS complex
represents activation of the ventricles through the normal AV
conduction system.
Clinical Significance
Preexcitation of the ventricles is an electrocardiographic di-
agnosis characterized by the presence of a short PR interval
and a delta wave. This specific pattern of preexcitation is also
called the WPW ECG. Not all patients with the WPW ECG
will develop symptoms of tachycardia. When preexcitation of
the ventricles is associated with symptoms of tachycardia, the
clinical entity is called WPW syndrome.
The bypass tract can be right sided (connecting the right
atrium to the right ventricle anywhere within the tricuspid
ring) or left sided (connecting the left atrium to the left ven-
tricle anywhere within the mitral ring). It may be located an-
teroseptally, posteroseptally, or laterally at the free wall of the
left or right ventricle. More than half of bypass tracts are lo-
cated at the left lateral free wall connecting the left atrium to
the left ventricle, about 20% to 30% are posteroseptal in lo-
cation, 10% to 20% are at the right lateral wall connecting
the right atrium to the right ventricle, and the remaining 5%
are anteroseptal in location. Anteroseptal bypass tracts are
mainly right sided.
Wolff-Parkinson-White Syndrome 271
The bypass tract may be single or multiple. Conduction may
be fixed or intermittent and may be anterograde only
(atrium to ventricle), retrograde only (ventricle to atrium) or
both. Ventricular preexcitation therefore can manifest in dif-
ferent patterns and can be mistaken for other abnormalities
not only during normal sinus rhythm, but also during tachy-
cardia. Accordingly, preexcitation of the ventricle can be mis-
taken for left or right bundle branch block; left or right ven-
tricular hypertrophy; posterior, inferior, anterior, and lateral
Q wave myocardial infarction; non-Q wave myocardial in-
farction; myocardial ischemia; or other repolarization ab-
normalities. It can also be mistaken for ectopic beats or in-
termittent bundle branch block. The WPW ECG therefore is
a great masquerader of several ECG abnormalities.
The 12-lead ECG is helpful in localizing the bypass tract dur-
ing normal sinus rhythm. The more prominent the delta
wave (or the greater the ventricular preexcitation), the more
accurate is the localization. The location of the bypass tract
during normal sinus rhythm should be compared with the
location of the bypass tract during tachycardia. This may
help identify if more than one bypass tract is present.
Approximately 10% to 20% of patients with Ebsteins anom-
aly has WPW syndrome with more than one bypass tract
commonly present. In Ebsteins anomaly, the right ventricle
is atrialized because of a downward displacement of the tri-
cuspid leaflets into the right ventricle; thus, Ebsteins anom-
aly should always be suspected when a bypass tract is right
sided. Other cardiac diseases associated with preexcitation
include hypertrophic cardiomyopathies and mitral valve
prolapse.
The presence of preexcitation can cause auscultatory changes
in the heart.
Right-sided bypass tract: If the bypass tract is right
sided, the right ventricle is activated earlier than the left
ventricle. Delay in activation of the left ventricle will
cause a softer first heart sound. Earlier activation of the
right ventricle will cause earlier closure of the pulmonic
component of the second sound, which can result in a
single or paradoxically split second heart sound.
Left-sided bypass tract: If the bypass tract is left sided,
the left ventricle is activated earlier than the right ventri-
cle. This can cause the first heart sound to be accentuated.
Delay in activation of the right ventricle will cause the
pulmonic second sound to be further delayed resulting in
wide splitting of the second heart sound. These ausculta-
tory findings become audible only when a significant por-
tion of the QRS complex is contributed by the bypass
tract.
Treatment and Prognosis
Asymptomatic patients: The presence of preexcitation in
the baseline ECG may not be associated with symptoms and
may be discovered unexpectedly during a routine ECG for
reasons unrelated to symptoms of tachycardia.
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272 Chapter 20

Figure 20.16: Conduction across

the Bypass Tract. (A) The bypass
Atria Atria Atria
tract can conduct only anterogradely
from atrium to ventricle (dotted arrow);
(B) only retrogradely, from ventricle to
atrium; and (C), both anterogradely
and retrogradely, from atrium to ventri-
cle and from ventricle to atrium.
Ventricles Ventricles Ventricles

A B C
Anterograde Retrograde Both anterograde
conduction only conduction only and retrograde
conduction

Among asymptomatic patients with intermittent preexci- AV reciprocating tachycardia or AVRT

tation, without structural or congenital heart disease who
continue to remain completely asymptomatic, the preex-
citation may disappear, with a good prognosis. Routine
electrophysiologic testing is not recommended.
Among asymptomatic patients with ECG pattern of pre-
excitation that is fixed or constant, the prognosis will
depend on the physiologic characteristics and refrac-
tory period of the accessory pathway. The American
College of Cardiology/American Heart Association
(ACC/AHA) Task Force on Practice Guidelines for
Clinical Intracardiac Electrophysiologic and Catheter
Ablation Procedures does not recommend routine elec-
trophysiologic testing in asymptomatic patients with
preexcitation except those with a family history of sud-
den death or patients who are engaged in high-risk oc-
cupations or activities.
Symptomatic patients: In patients with classical preexci-
tation manifested by short PR interval and delta wave asso-
ciated with clinical symptoms of tachycardia, the overall
prognosis remains good except that there is an approximate
0.15% to 0.39% chance of sudden cardiac death occurring
over a 3- to 10-year follow-up. The ACC/AHA/European
Society of Cardiology (ESC) guidelines for the management
of patients with supraventricular arrhythmias consider ab-
lation therapy as Class I indication for patients with acces-
sory pathways that are symptomatic. Antiarrhythmic ther-
apy in these patients receives a Class IIa recommendation.
Arrhythmias Associated with the
WPW Syndrome
One of the clinical features of the WPW syndrome is its
predisposition to develop arrhythmias. The following
are the most important arrhythmias associated with
the WPW syndrome:
n Orthodromic or narrow complex AVRT
n Antidromic or wide complex AVRT
Atrial fibrillation
The electrophysiologic characteristics of the bypass tracts
are highly variable. Some bypass tracts can conduct only
anterogradely from atrium to ventricle (Fig. 20.16A),
some only retrogradely from ventricle to atrium (Fig.
20.16B), and others can conduct both anterogradely
from atrium to ventricle and retrogradely from ventricle
to atrium (Fig. 20.16C). This may influence the type of
arrhythmia associated with the WPW syndrome.
Narrow Complex and Wide Complex
AV Reciprocating Tachycardia
AV reciprocating tachycardia (AVRT): AVRT is the
most common arrhythmia associated with the WPW
syndrome. AVRT is a supraventricular tachycardia that
may have narrow or wide QRS complexes. The QRS
complexes may be narrow or wide depending on how
the ventricles are activated during the tachycardia.
Narrow complex AVRT: This type of AVRT has nar-
row QRS complexes because the atrial impulse enters
the ventricles anterogradely through the AV node
during tachycardia (Fig. 20.17A). The impulse fol-
lows the intraventricular conduction system and acti-
vates the ventricles, normally resulting in QRS com-
plexes that are identical to that during normal sinus
rhythm. This type of AVRT is also called orthodromic
or narrow complex AVRT and was discussed in Chap-
ter 16, Supraventricular Tachycardia due to Reentry.
Wide Complex AVRT: This type of AVRT has wide
QRS complexes because the atrial impulse enters
the ventricles through the bypass tract during the
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Wolff-Parkinson-White Syndrome 273

A B

Orthodromic AVRT Antidromic AVRT

Figure 20.17: Orthodromic and Antidromic AVRT. (A) Orthodromic AVRT. During
tachycardia, the impulse is conducted from atrium to ventricle across the AV node resulting
in narrow QRS complexes. (B) Antidromic AVRT. During tachycardia, the atrial impulse is
conducted from atrium to ventricle across the bypass tract resulting in wide QRS complexes,
which can be mistaken for ventricular tachycardia. AVRT, atrioventricular reciprocating
tachycardia.

tachycardia (Fig. 20.17B). The impulse activates the
ventricles outside the normal conduction system re-
sulting in wide QRS complexes, which can be mis-
taken for ventricular tachycardia. Wide complex
AVRT is also called antidromic AVRT and is further
discussed in this chapter.
Narrow Complex or Orthodromic AVRT
Mechanism of narrow complex AVRT. Narrow com-
plex AVRT is discussed in more detail in Chapter 16. The
tachycardia is triggered by a premature atrial or ventricu-
lar impulse. Figure 20.18 illustrates how a premature
atrial impulse can precipitate a narrow complex AVRT.
The premature atrial impulse should be perfectly
timed to occur when the AV node has fully recov-
ered from the previous impulse while the bypass
tract is still refractory. Because the AV node has a
shorter refractory period, the premature atrial im-
pulse is able to conduct through the AV node, but is
blocked at the bypass tract (Fig. 20.18A).
The ventricles are activated through the normal
AV conduction system, resulting in a narrow QRS

Sinus Rhythm AVRT No delta waves

Delta PAC during tachycardia
wave

PAC
Atria
Bypass
By tract AV node
tra AV node conducts
has a conducts
lon impulse
ref shorter impulse from
from
pe refractory
ventricle to
atria to
period ventricles
atrium

Ventricles
A B C

Figure 20.18: Orthodromic or Narrow Complex AVRT. (A) A premature atrial complex
(PAC) is conducted through the AV node but not through the bypass tract. (B) The ventricles are
activated exclusively through the normal conduction system causing the QRS complex to be
narrow. (C) The impulse is conducted from ventricles to atria across the bypass tract. The atria
are activated retrogradely allowing the impulse to be conducted back to the ventricles through
the AV node. Note that delta waves are present only during normal sinus rhythm but not during
tachycardia. AV, atrioventricular; AVRT, atrioventricular reciprocating tachycardia.
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274 Chapter 20
Sinus Rhythm PAC
PAC
Atria
Bypass
tract has AV node
a shorte has a
refractor longer
period refractory
period
A V
Figure 20.19: Antidromic or Wide Complex AVRT. (A) A premature atrial complex (PAC) is con-
ducted through the bypass tract but not through the AV node. (B) The QRS complex is wide because
the ventricles are activated outside the normal conduction system. (C) The impulse is conducted retro-
gradely from ventricles to atria through the atrioventricular conduction system. The atria are activated
retrogradely allowing the impulse to be conducted back to the bypass tract. AVRT, atrioventricular re-
ciprocating tachycardia.
complex (Fig. 20.18B). After the ventricles are acti-
vated, the impulse is conducted retrogradely from
ventricle to atrium across the bypass tract. After the
atria are activated, the impulse can reenter the AV
node resulting in a narrow complex tachycardia called
orthodromic AVRT (Fig. 20.18C). Delta waves are not
present during tachycardia because activation of the
ventricles occurs exclusively through the AV node.
Wide Complex or Antidromic AVRT
Mechanism of wide complex AVRT: Antidromic or
wide complex AVRT is triggered by a premature im-
pulse originating from the atria or ventricles. The dia-
gram illustrates how the tachycardia is initiated (Fig.
20.19).
The premature atrial impulse should be perfectly
timed to occur when the bypass tract has fully re-
covered from the previous impulse while the AV
node is still refractory. Because the bypass tract has a
shorter refractory period, the premature atrial im-
pulse will enter the bypass tract but is blocked at the
AV node (Fig. 20.19A).
The atrial impulse activates the ventricles through
the bypass tract (Fig. 20.19B). The impulse spreads
from one ventricle to the other by muscle cell to
muscle cell conduction, causing a wide QRS com-
Antidromic AVRT
Bypass
AV node
tract
conducts
conducts
impulse
impulse
from
from atria
ventricles
to
to atria
ventricles
plex. The impulse is conducted retrogradely to the
atria across the AV conduction system. The atria are
activated retrogradely, thus completing the circuit.
The atrial impulse can again reenter the bypass tract
and the circuit starts all over again (Fig. 20.19C).
Conduction Pathways in
Antidromic AVRT
Wide complex AVRT: There are two types of wide
complex AVRT:
Ventriculoatrial conduction across the AV
node: In wide complex AVRT, anterograde conduc-
tion of the atrial impulse to the ventricles occurs
through the bypass tract and retrograde conduction
of the impulse from ventricles to atria occurs
through the AV node (Fig. 20.20A). This wide com-
plex AVRT is called type I antidromic AVRT. This
type of wide complex tachycardia may be termi-
nated by vagal maneuvers and AV nodal blockers be-
cause the AV node is part of the reentrant circuit.
Ventriculoatrial conduction across another by-
pass tract: Retrograde conduction of the ventricu-
lar impulse to the atria may occur through a second
bypass tract instead of the AV node, although this is
extremely rare (Fig. 20.20B). This wide complex
AVRT is called type II. Type II wide complex AVRT
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Wolff-Parkinson-White Syndrome 275

A B

Type I: VA conduction Type II: VA conduction

across AV Node across another bypass tract

Figure 20.20: VA Conduction in Antidromic AVRT. (A) In type I antidromic

AVRT, the atrial impulse enters the ventricles through the bypass tract and returns to
the atria through the AV node. This type of antidromic AVRT can be terminated by AV
nodal blockers. (B) In type II antidromic AVRT, the impulse enters the ventricles
through the bypass tract and returns to the atria through a second bypass tract. This
type of antidromic AVRT cannot be terminated by AV nodal blockers. Both wide com-
plex tachycardia look identical and can be mistaken for ventricular tachycardia. AV,
atrioventricular; VA, ventriculoatrial; AVRT, atrioventricular reciprocating tachycardia.

can not be terminated by vagal maneuvers or AV
nodal blockers because the AV node is not part of
the reentrant circuit. The ECG of type I and type II
wide complex AVRT are identical showing wide
QRS complexes.
Localizing the bypass tract during wide complex
AVRT: The ventricular insertion of the bypass tract can
be localized during a wide complex tachycardia.
Right bundle branch block configuration: If the
wide complex AVRT has a right bundle branch
block configuration (R waves are taller than S waves
in V1), the bypass tract is left sided. During tachycar-
dia, the left ventricle is activated earlier than the
right ventricle. Thus, the impulse spreads from left
ventricle to right ventricle causing a tall QRS com-
plex in V1 (Fig. 20.21A).

V1
V1
Right sid
bypass
Left sided tract
bypass
tract

B
A

Figure 20.21: Localizing the Bypass Tract during Wide Complex AVRT. (A) When
the bypass tract is left sided (bypass tract connects left atrium to left ventricle), tall R waves
are recorded in V1 during wide complex tachycardia. Because the left ventricle is activated
first, the impulse will travel from left ventricle to right ventricle toward V1. (B) If the bypass
tract is right sided, the right ventricle is activated first and the impulse is conducted from
right ventricle to left ventricle causing deep S waves in V1. AVRT, atrioventricular reciprocat-
ing tachycardia.
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276 Chapter 20
Left bundle branch block configuration: If the
wide complex AVRT has a left bundle branch block
configuration (S waves are deeper than the R waves
in V1), the bypass tract is right sided. During wide
complex AVRT, the right ventricle is activated earlier
that the left ventricle. Thus, the ventricular impulse
spreads from right ventricle to left ventricle causing
a negative complex in V1 (Fig. 20.21B).
Figure 20.22 is from a patient with right-sided bypass
tract. During wide complex AVRT (Fig. 20.22B), the
QRS complexes have a left bundle branch block config-
uration consistent with a right-sided bypass tract. Dur-
ing narrow complex AVRT (Fig. 20.22C,D), the retro-
grade P waves are upright in leads I and aVL, which is
also consistent with a right-sided bypass tract. The lo-
cation of the bypass tract during narrow complex
AVRT matches the location of the bypass tract during
wide complex AVRT and during normal sinus rhythm.
If the location of the bypass tract during tachycardia
and during normal sinus rhythm does not match, more
than one bypass tract may be present.
Figures 20.22C,D are from the same patient as Figures
20.22A, B. Retrograde P waves (arrows) are upright in
leads I and aVL during narrow complex AVRT consis-
tent with right-sided bypass tract.
Antidromic or Wide Complex AVRT
Another example of wide complex AVRT is shown in
Fig. 20.23. The QRS complexes are tall in V1 consistent
with a left-sided bypass tract.
Wide Complex AVRT
Treatment: The reentrant pathway during wide com-
plex AVRT generally involves the same structures as
that during narrow complex AVRT. Thus, vagal ma-
neuvers and AV nodal blockers are usually effective in
terminating the tachycardia (Fig. 20.24A). Before AV
nodal blocking agents are given, it should be ascer-
tained that the wide complex tachycardia is not ven-
tricular tachycardia because catastrophic results may
occur if the tachycardia turns out to be ventricular
rather than supraventricular. Furthermore, adenosine,
which is a very effective agent in converting AVRT to
normal sinus rhythm, can cause atrial fibrillation in up
to 10% of patients. This may be catastrophic if the pa-
tient has preexcitation. Additionally, if the wide com-
plex AVRT uses a second bypass tract for ventriculoa-
trial conduction (type II wide complex AVRT), AV nodal
blockers will not be effective in terminating the tachycar-
dia because the AV node is not part of the reentrant path-
way. Thus, ibutilide, procainamide, or flecainide, which
are capable of blocking the reentrant circuit at the level of
the bypass tract (Fig. 20.24B), are the preferred agents ac-
cording to the ACC/AHA/ESC guidelines in the manage-
ment of patients with supraventricular arrhythmias.
ECG Findings of Antidromic or Wide
Complex AVRT
1. The QRS complexes are wide measuring 120 milliseconds.
The tachycardia is difficult to distinguish from ventricular
tachycardia.
2. The tachycardia is very regular because the tachycardia uses a
fixed reentrant circuit.
3. AV block is not possible because the atria and ventricles are
part of the reentrant pathway.
4. Although retrograde P waves are present, similar to ortho-
dromic AVRT, the P waves can not be identified because they
are obscured by the ST segment.
Mechanism
AVRT is possible only when a bypass tract is present. For
tachycardia to occur, the AV node and bypass tract should
have different electrophysiologic properties. The tachycardia
can be triggered by a premature atrial or ventricular impulse
and can be narrow complex (orthodromic) or wide complex
(antidromic).
Orthodromic or narrow complex AVRT: If the bypass
tract has a longer refractory period than the AV node, a per-
fectly timed premature atrial impulse is blocked at the by-
pass tract, but is conducted to the AV node and His-Purkinje
system, resulting in a narrow complex or orthodromic
AVRT. Unlike the baseline ECG in which delta waves are
present due to preexcitation, there are no delta waves dur-
ing the tachycardia because the ventricles are activated ex-
clusively from the AV node. This tachycardia was already
discussed in Chapter 16, Supraventricular Tachycardia due
to Reentry.
Antidromic or wide complex AVRT: If the AV node has
a longer refractory period than the bypass tract, a prema-
ture atrial impulse can enter the bypass tract but not the
AV node, resulting in wide complex or antidromic AVRT.
In antidromic AVRT, the premature atrial impulse is con-
ducted through the bypass tract and activates the ventri-
cles by direct myocardial spread resulting in a wide QRS
complex. The ventricular impulse is conducted retro-
gradely to the atria across the AV node and reenters the
ventricles through the bypass tract. The reentrant tachy-
cardia involves a large circuit consisting of the bypass
tract, ventricles, bundle branches, bundle of His, AV
node, and atria before circling back to the bypass tract to
activate the ventricles. Because the ventricles are activated
exclusively from the bypass tract, the whole QRS complex
is not a fusion complex and is essentially a delta wave.
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Figure 20.22: (A) Baseline Electrocardiogram (ECG) Showing Preexcitation. Delta waves with short PR
intervals are present in leads I, aVL, V2, and V3 consistent with preexcitation.The QRS complex is negative in V1 with
deep S waves consistent with a right sided bypass tract. (B) Wide Complex AVRT. The 12-lead ECG is from the same
patient as (A). It shows a wide complex tachycardia with deep S wave in V1 suggesting that the bypass tract is right
sided.This wide complex tachycardia can be mistaken for VT. (C) Narrow complex tachycardia. The ECG shows nar-
row complex AVRT.The frontal leads are magnified in (D) to show that the retrograde P waves (arrows) are upright
in I and aVL consistent with a right-sided bypass tract. (continued)

277
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278 Chapter 20
Figure 20.22: (Continued) (D) Narrow complex AVRT. The ECG is from (C). Only the frontal leads are magnified to
show that the P waves are upright in leads I and aVL during SVT. AVRT, atrioventricular reciprocating tachycardia;
SVT, supraventricular tachycardia.
Clinical Significance
Narrow complex AVRT is the most common arrhythmia in
patients with the WPW syndrome occurring in approxi-
mately 85% to 95% of patients who have symptoms of tachy-
cardia. Wide complex AVRT is rare, occurring only in 5% to
10% of patients with WPW syndrome. Antidromic or wide
complex AVRT is a classic example of wide complex tachy-
cardia of supraventricular origin.
Wide complex AVRT is difficult to differentiate from ventric-
ular tachycardia because both arrhythmias have wide QRS
complexes. Ventricular tachycardia usually occurs in patients
with history of myocardial infarction or left ventricular sys-
tolic dysfunction. Wide complex AVRT occurs in patients who
are younger with known preexcitation and generally preserved
left ventricular systolic function. The ECG algorithm for diag-
nosing wide complex tachycardia of ventricular origin is fur-
ther discussed in Chapter 22, Wide Complex Tachycardia.
The ventricular insertion of the bypass tract can be localized
Treatment
during wide complex tachycardia. The bypass tract is left
sided if the QRS complexes have a right bundle branch block
configuration (R waves are taller than S waves in V1). If the
QRS complexes have a left bundle branch block configura-
tion (S waves are deeper than the height of the R waves in
V1), the bypass tract is right sided.
Although it can be assumed that patients with preexcitation
who develop narrow complex tachycardia have AVRT as the
cause of the tachycardia, in more than 5% of patients with
preexcitation, the narrow complex tachycardia is due to AV
nodal reentrant tachycardia rather than AVRT. The exact
mechanism of the tachycardia is important if radiofrequency
ablation is being considered.
Patients with Ebstein anomaly may have more than one by-
pass tract. These patients may not respond to AV nodal
blockers during wide complex AVRT because the AV node
may not be part of the reentrant pathway. Similarly, ablation
therapy may not be as effective because several bypass tracts
may be present.
Wide or narrow complex AVRT is paroxysmal with abrupt
onset and sudden termination. During tachycardia, promi-
nent jugular venous pulsations from cannon A waves are
usually seen in the neck. These jugular pulsations are due to
synchronous contraction of both atria and ventricles.
Wide complex tachycardia of uncertain diagnosis: Wide
complex AVRT may be difficult to differentiate from ventric-
ular tachycardia. If the diagnosis of the wide complex tachy-
cardia is uncertain and there is possibility that the tachycar-
dia is ventricular rather than supraventricular, AV nodal
blockers, especially verapamil, should be avoided. Verapamil
is negatively inotropic and a potent vasodilator. If verapamil is
inadvertently given to a patient with ventricular tachycardia,
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Wolff-Parkinson-White Syndrome 279

Figure 20.23: (A) Antidromic or Wide Complex AVRT. The 12-lead ECG shows a wide complex tachycardia
from antidromic AVRT. The QRS complexes show tall R waves in V1 consistent with a left-sided bypass tract. The tachycar-
dia can be mistaken for ventricular tachycardia. (B) After Conversion to Normal Sinus Rhythm. The 12-lead ECG is from
the same patient as (A). The rhythm is normal sinus.There are multiple leads showing short PR interval and delta waves
(arrows) consistent with ventricular preexcitation. Negative delta waves are present in III and aVF with tall R waves in
V1 consistent with a left-sided posteroseptal bypass tract. The location of the bypass tract during wide complex AVRT
matches that during normal sinus rhythm. AVRT, atrioventricular reciprocating tachycardia; ECG, electrocardiogram.

the patient may become hemodynamically unstable because
most patients with ventricular tachycardia have left ventricu-
lar systolic dysfunction. Additionally, AV nodal blockers
should not be given if there is irregularity in the R-R interval,
which may indicate atrial fibrillation with preexcitation. Fi-
nally, patients with preexcitation who develop wide complex
tachycardia may not be due to AVRT but may be due to focal
atrial tachycardia or atrial flutter conducting across a bypass
tract. This type of wide complex tachycardia will not respond
to AV nodal blockers. Agents that will slow conduction across
the bypass tract such as ibutilide, procainamide, or flecainide
given intravenously are preferred agents according to the
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280 Chapter 20
A: VA conduction
Figure 20.24: Effect of AV Nodal Block-
across AV Node
ers in Wide Complex AVRT. If the
retrograde pathway involves the AV node as
shown in (A), vagal maneuvers and AV nodal
Vagal Maneuvers
blockers will be effective in terminating the AV Nodal Blockers
tachycardia. However, if the AV node is not part Adenosine*
of the reentrant pathway (B), AV nodal block- -Blockers*
Ca Channel Blockers*
ers will not be effective in terminating the
Digitalis*
tachycardia. Antiarrhythmic agents that can
block the impulse at the bypass tract are the
preferred agents for terminating the tachycar-
dia. The asterisks indicate that the drugs are
available as intravenous preparations. VA, ven-
triculoatrial; AV, atrioventricular.
ACC/AHA/ESC guidelines for the management of patients
with supraventricular arrhythmias.
Wide complex AVRT: Wide complex AVRT can be termi-
nated by slowing conduction across the AV node or bypass
tract. The most vulnerable arm of the tachycardia circuit is
the AV node, which can be inhibited with vagotonic maneu-
vers such as Valsalva, carotid sinus pressure, immersion of
the face in cold water (diving reflex), gagging, coughing, or
straining. If vagotonic maneuvers are not effective, pharma-
cologic therapy should be considered among stable patients
and electrical cardioversion among patients who are not sta-
ble. Electrical cardioversion is also an option even among
stable patients, especially if the etiology or mechanism of the
wide complex tachycardia is uncertain.
Pharmacologic agents: AV nodal blockers and antiar-
rhythmic agents that inhibit conduction across the bypass
tract are both effective in terminating wide complex AVRT.
n Adenosine: Although adenosine is effective in termi-
nating AVRT, it is not the best agent when there is
wide complex AVRT for the following reasons:
n Adenosine can cause atrial fibrillation in up to 10%
of patients, which may be catastrophic in patients
with preexcitation. Thus, resuscitative equipment
should be available if adenosine is being given to a
patient with known WPW syndrome.
n There is a subset of antidromic AVRT in which AV
conduction of the impulse occurs through one by-
pass tract and ventriculoatrial conduction occurs
through another bypass tract. AV nodal blockers
such as adenosine will not be effective because this
type of AVRT does not use the AV node as part of
the reentrant circuit.
n Finally, there are other supraventricular arrhyth-
mias such as focal atrial tachycardia and atrial
flutter that can result in wide complex tachycar-
dia when a bypass tract is present. These arrhyth-
mias will conduct to the ventricles across the by-
B: VA conduction across
another bypass tract
Type I A
Procainamide*
Quinidine
Disopyramide
Type I C Type III
Propafenone Ibutilide*
Flecainide Sotalol
Amiodarone*
pass tract and will not respond to adenosine be-
cause the AV node is not involved with the tachy-
cardia. Thus, antiarrhythmic agents that can slow
the impulse at the bypass tract are preferred
agents.
n Antiarrhythmic agents: According to the ACC/
AHA/ESC guidelines for the management of patients
with supraventricular arrhythmias, antiarrhythmic
agents that block the bypass tract are more effective
and are preferred in the acute treatment of wide com-
plex AVRT. This includes procainamide, ibutilide, or
flecainide. Flecainide is not available intravenously in
the United States.
n Procainamide: Procainamide is the drug of choice
and is given intravenously to a total dose of 10 to
12 mg/kg, not to exceed 1,000 mg. The dose is
given within 30 minutes at the rate of 100 mg every
2 to 3 minutes followed by a maintenance infusion
of 1 to 4 mg/minute.
n Ibutilide: One mg is given intravenously over 10
minutes. The 10-mL solution can be injected
slowly IV or diluted with D5W to a total volume of
100 mL and infused over 10 minutes. If the wide
complex AVRT has not converted to normal sinus
rhythm after 10 minutes, the same dose is re-
peated. Experience with ibutilide is not as exten-
sive as that with procainamide although the drug
may be as effective.
n Other antiarrhythmic agents: Other Class IA (quini-
dine and disopyramide) IC (propafenone) and Class
III agents (sotalol) are not available as intravenous
preparations, but are effective for long-term therapy
by inhibiting the bypass tract. These agents are nega-
tively inotropic and should not be given when there is
left ventricular dysfunction or heart failure. If the pa-
tient has left ventricular systolic dysfunction, amio-
darone is the preferred agent. Amiodarone, however,
LWBK271-C20_262-286.qxd 1/29/09 1:43 PM Page 281 LWBK271-C01_01-08.qxd
has not been shown to be more effective than other
agents and has several long-term toxic effects and is
reserved in the treatment of patients with structural
cardiac disease.
Electrical cardioversion: Electrical cardioversion is
reserved for patients who are hemodynamically unsta-
ble with hypotension, congestive heart failure, or with
symptoms of ischemia from tachycardia. It is also an
initial option to patients who are hemodynamically
stable. It should also be considered if the patient does
not respond to initial pharmacologic therapy or when
the diagnosis of the wide complex tachycardia remains
uncertain. In stable patients, a low energy setting is
generally adequate in terminating the tachycardia (50
joules).
Intracardiac pacing: The tachycardia can also be ter-
minated by a perfectly timed premature atrial complex
or premature ventricular complex because the atria and
ventricles are part of the reentrant circuit. Before the
era of radiofrequency ablation, insertion of permanent
pacemakers with antitachycardia properties has been
used in the treatment of both antidromic and ortho-
dromic AVRT. The device can detect the tachycardia
and paces the atria or ventricles to interrupt the
arrhythmia.
Radiofrequency ablation: Radiofrequency ablation of
the bypass tract using catheter techniques is now the pre-
ferred therapy and receives a Class I recommendation in
symptomatic patients with preexcitation especially in
younger individuals to obviate the need for long-term an-
tiarrhythmic therapy. The procedure is usually very effec-
tive with more than 95% chance of cure. If radiofre-
quency ablation is not technically feasible, ablation
surgery should be considered.
Prognosis
Patients with preexcitation who develop symptoms from
tachycardia, overall prognosis remains good. These patients
should be referred to an electrophysiologist for further eval-
uation with a chance for complete cure.
Atrial Fibrillation
Atrial fibrillation is one of the most dreadful arrhyth-
mias associated with WPW syndrome. This arrhythmia
has the potential of degenerating to ventricular fibrilla-
tion, which can result in sudden cardiac death. The
ECG findings of atrial fibrillation in the presence of
preexcitation are:
Irregularly irregular R-R intervals.
Varying morphologies of the QRS complexes.
The ventricular rate is usually rapid.
Wolff-Parkinson-White Syndrome 281
During atrial fibrillation, the atrial impulses can reach
the ventricles through both AV node and bypass tract
resulting in varying degrees of ventricular fusion. Be-
cause the bypass tract consists of ordinary myocardium,
it can allow atrial complexes to enter the ventricles re-
sulting in very rapid ventricular rates (Fig. 20.25).
Atrial fibrillation degenerating to ventricular fibrilla-
tion is rare, even among symptomatic patients with
WPW syndrome. Atrial fibrillation however carries the
potential for sudden death. Patients with WPW syn-
drome with bypass tracts that are capable of conducting
at rates 240 beats per minute (R-R interval between
two preexcited complexes 250 milliseconds or 6
small blocks) are at risk for sudden death as shown in
Figures 20.25 and 20.26.
Atrial Fibrillation in Patients with
WPW Syndrome
Treatment: The standard treatment of atrial fibrilla-
tion is to slow the ventricular rate with AV nodal block-
ing agents such as calcium channel blockers, beta block-
ers, and digoxin. In patients with preexcitation, the use
of these agents is not only contraindicated, but also may
be catastrophic. AV nodal blockers slow down conduc-
tion and decrease the number of impulses entering the
ventricles anterogradely through the AV node. This will
reduce the number of impulses bombarding the ven-
tricular end of the bypass tract, rendering the bypass
tract less refractory (Fig. 20.27). Calcium channel
blockers can also cause peripheral vasodilatation, which
may result in reflex increase in sympathetic tone. This
may increase conduction through the bypass tract. The
use of digitalis is particularly dangerous because digi-
talis does not only block the AV node, but also enhances
conduction through the bypass tract.
Electrical cardioversion is the treatment of choice in
patients with atrial fibrillation who are unstable. In sta-
ble patients, procainamide is the pharmacologic agent
of choice. Ibutilide, amiodarone, propafenone, and so-
talol are also effective. These agents can slow the ventric-
ular rate but can also convert atrial fibrillation to sinus
rhythm.
Atrial Fibrillation and WPW
Syndrome
ECG Findings of Atrial Fibrillation
and WPW Syndrome
1. The R-R intervals are irregularly irregular.
2. The ventricular rate is unusually rapid.
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282 Chapter 20

Atrial
Fibrillation

AV Node Bypass
tract

Narrow Complexes

Figure 20.25: Atrial Fibrillation and the WPW Syndrome. In patients with WPW
syndrome with atrial fibrillation, atrial impulses can enter the ventricles through both bypass
tract and AV node. Note that in the middle of the rhythm strip, narrow QRS complexes are
present (bracket). These impulses are conducted through the AV node. The wide QRS
complexes (arrows) are preexcited and are conducted through the bypass tract. Some QRS
complexes are fusion complexes due to activation of the ventricles from both bypass tract
and AV node. The R-R interval between two wide QRS complexes measure 250 milliseconds
(distance between the two arrows) making the patient high risk for ventricular fibrillation.
WPW, Wolff-Parkinson-White; AV, atrioventricular.

3. The QRS complexes have different configurations, some nar-
row, some wide, and others in between.
Mechanism
When atrial fibrillation occurs in a patient without a by-
pass tract, atrial impulses can reach the ventricles only
through the AV node because this is the only pathway that
connects the atria to the ventricles. Accordingly, the ven-
tricular rate is usually controlled because the capacity of
the AV node to transmit atrial fibrillatory impulses to the
ventricles is limited.
When atrial fibrillation occurs in a patient with WPW syn-
drome, the bypass tract serves as a second pathway, in addi-
tion to the AV node, for atrial impulses to reach the ventri-
cles. Because the bypass tract consists of ordinary
myocardium, it is capable of conducting atrial impulses
more rapidly to the ventricles than the AV node, resulting in
very rapid ventricular rates, which can degenerate to ventric-
ular fibrillation and sudden death.
The QRS complexes have varying configurations because
two separate pathways are involved in conducting atrial im-
pulses to the ventricles. Wide QRS complexes occur when
atrial impulses are conducted through the bypass tract and
narrow complexes are present when the AV node and con-
duction system transmit atrial impulses to the ventricles. In
addition, fusion complexes of varying configurations are
present when the AV node and bypass tract simultaneously
contribute to ventricular activation.
Clinical Implications
Atrial fibrillation is the most serious arrhythmia associated
with WPW syndrome. The arrhythmia can result in very
rapid ventricular responses, which can lead to hypotension,
diminished coronary perfusion, and ventricular fibrillation.
This may cause sudden death even in healthy individuals.
Approximately 30% to 40% of patients with preexcitation
with symptoms of tachycardia will develop atrial fibrillation.
The presence of AVRT increases the incidence or predisposi-
tion to develop atrial fibrillation, which (in the presence of
preexcitation) may degenerate to ventricular fibrillation. Con-
versely, in patients with AVRT, successful ablation of the acces-
sory pathway will diminish the incidence of atrial fibrillation.
It is possible that completely asymptomatic patients with
preexcitation may suddenly develop atrial fibrillation as the
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Wolff-Parkinson-White Syndrome 283

A.

B.

Figure 20.26: Atrial Fibrillation and WPW Syndrome. ECG (A) shows atrial fibrillation in a patient with
known WPW syndrome. Note the irregularly irregular R-R intervals and the presence of bizarre QRS complexes of
varying morphologies. The R-R interval between both preexcited complexes measures 250 milliseconds, making
patient high risk for ventricular fibrillation. (B) From the same patient upon conversion to normal sinus rhythm. ECG
(B) shows preexcitation. The patient underwent successful ablation of a left-sided posteroseptal bypass tract. ECG,
electrocardiogram; WPW, Wolff-Parkinson-White.

initial symptom degenerating to ventricular fibrillation, al-
though this is exceedingly rare. Electrophysiologic testing in
patients who are asymptomatic is not necessary, as previ-
ously discussed.
Patients with preexcitation who are symptomatic have a
higher chance of developing atrial fibrillation, although
the chance that the atrial fibrillation can degenerate to
ventricular fibrillation is also rare. Patients with preexcita-
tion who are symptomatic should be risk stratified so that
those who are high risk for cardiac sudden death can be
identified.
The following markers suggest that the patient is low risk
for sudden death.
n Patients with preexcitation in the resting ECG, but are
completely asymptomatic.
n The preexcitation is noted only intermittently during
routine ECG.
n There is immediate disappearance of preexcitation
during stress testing.
n The delta waves disappear when procainamide is
given intravenously.
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284 Chapter 20

A B

Bypass
AV ract pass
AV Nodal ct
Node
Blockers
More
inhibition Less
inhibition

Figure 20.27: Atrial Fibrillation and the WPW Syndrome. (A) During atrial fib-
rillation, atrial impulses can enter the ventricles through the AV node and bypass tract.
Atrial impulses entering the AV node can activate the ventricles and at the same time
depolarize the ventricular end of the bypass tract retrogradely (arrows). This can render
the bypass tract refractory, thus slowing down the number of atrial impulses entering
the ventricles through the bypass tract. (B) When AV nodal agents are given, the number
of atrial impulses entering the AV node is decreased. This will also decrease the number
of impulses depolarizing the ventricular end of the bypass tract. Because there is less in-
hibition of the ventricular end of the bypass tract, the bypass tract is less refractory and
will allow more atrial impulses to enter the ventricles through the bypass tract antero-
gradely. AV, atrioventricular; WPW, Wolff-Parkinson-White.

The following are markers of a high-risk patient. These
observations suggest that the bypass tract has a short re-
fractory period and is capable of conducting atrial im-
pulses rapidly.
n The delta wave persists during stress testing.
n The refractory period of the bypass tract is short meas-
uring 250 milliseconds between preexcited com-
plexes. This can be measured during spontaneously oc-
curring atrial fibrillation or it can be induced in the
electrophysiology lab during electrophysiologic testing.
n History of cardiac arrest from ventricular fibrillation.
n Presence of multiple accessory pathways.
n Presence of Ebstein anomaly.
Treatment
Treatment of atrial fibrillation in patients with WPW syn-
drome associated with wide QRS complexes includes direct
current cardioversion, use of antiarrhythmic agents, and ra-
diofrequency ablation.
Direct current cardioversion: In hemodynamically unsta-
ble patients associated with rapid ventricular rates, direct
current cardioversion receives a Class I recommendation. It
carries a Class II a recommendation among patients who are
stable according to the 2006 ACC/AHA/ESC guidelines in
the management of patients with atrial fibrillation.
Antiarrhythmic agents: In patients with atrial fibrillation
who are not hemodynamically unstable and do not need to
be cardioverted, pharmacologic agents that block the bypass
tract can be given as initial therapy.
Procainamide: Procainamide is the drug of choice and is
given intravenously at a dose of 10 to 12 mg/kg within 30
minutes at the rate of 100 mg every 2 to 3 minutes, not to ex-
ceed 1,000 mg. This is followed by a maintenance infusion
of 1 to 4 mg/minute. This is effective not only in slowing the
ventricular rate, but also in converting atrial fibrillation to
normal sinus rhythm in more than 50% of patients with
atrial fibrillation. This drug carries a Class I indication ac-
cording to the 2006 ACC/AHA/ESC practice guidelines.
Ibutilide: One mg of ibutilide is given IV slowly over 10
minutes and repeated if needed after an interval of 10 min-
utes. Ibutilide can block both bypass tract and AV node.
This is effective in converting atrial fibrillation to normal
sinus rhythm and also carries a Class I recommendation.
Flecainide: Intravenous flecainide receives a Class IIa rec-
ommendation in stable patients with atrial fibrillation with
rapid ventricular rates with wide QRS complexes. The intra-
venous dose is 1.5 to 3.0 mg/kg over 10 to 20 minutes. This
agent is not available intravenously in the United States.
Other antiarrhythmic agents: Amiodarone, quinidine,
and disopyramide can also inhibit the bypass tract and
carry a Class IIb recommendation. Only amiodarone is
available intravenously. The other agents are not available
as IV preparations in the United States.
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Wolff-Parkinson-White Syndrome 285

In patients with preexcitation, AV nodal blocking agents are
contraindicated and may be fatal when there is atrial fibrilla-
tion. AV nodal blocking agents decrease the number of im-
pulses entering the ventricles through the AV node, making
the bypass tract less refractory. It can also enhance conduc-
tion across the bypass tract. This will allow more fibrillatory
impulses to pass through the bypass tract from atrium to ven-
tricle, thus increasing the ventricular rate during atrial fibrilla-
tion. Digoxin is particularly a dangerous pharmacologic agent
to use in patients with WPW syndrome with atrial fibrillation.
Digoxin not only blocks the AV node, but also enhances con-
duction through the bypass tract, further increasing the ven-
tricular rate during atrial fibrillation. Verapamil also inhibits
the AV node and is a potent vasodilator. It may enhance con-
duction through the bypass tract by reflex increase in sympa-
thetic tone. These agents receive a Class III recommendation.
In patients with concealed bypass tracts (no evidence of pre-
excitation in baseline ECG) who develop atrial fibrillation,
the treatment of atrial fibrillation is similar to a patient with-
out a bypass tract. AV nodal blocking agents such as beta
blockers, calcium channel blockers, and digitalis can be given
safely in controlling the ventricular rate during atrial fibrilla-
tion. The use of digitalis as long-term maintenance therapy,
however, should be discouraged unless other AV nodal
blocking agents are ineffective or are poorly tolerated.
Some patients may be mistakenly identified as having con-
cealed bypass tracts because they do not manifest any evidence
of preexcitation in baseline ECG. These patients may not have
any preexcitation because the bypass tract is not given the
chance to become manifesteither from its distal location
from the sinus node (left-sided bypass tracts) or efficient con-
duction of the sinus impulse across the AV node. Anterograde
conduction of the atrial impulse to the ventricles may occur
during atrial fibrillation. These patients are difficult to identify
unless electrophysiologic testing is performed.
Prognosis
Prognosis is good even among patients with history of atrial
fibrillation because electrical ablation is curative. If radiofre-
quency ablation is not feasible, surgical ablation should be
considered.
Other Causes of Ventricular
Preexcitation
Ventricular preexcitation may be due to pathways other
than direct connection between the atrium and the
ventricle. The following summarizes the different path-
ways that can cause preexcitation.
Bundle of Kent: The bypass tract connects the
atrium directly to the ventricle (Fig. 20.28A). This is
the most common cause of preexcitation.
Mahaim fibers: Mahaim fibers may have different
connections:
n Nodoventricular connection: A bypass tract
connecting the AV node directly to the ventricle
(Fig. 20.28B).

Atria Atria Atria Atria

Ventricles Ventricles Ventricles Ventricles

A B C D

Figure 20.28: Other Causes of Preexcitation. (A) Preexcitation with a bypass tract con-
necting the atrium directly to the ventricles. This is associated with the classic ECG of WPW syn-
drome. (B) Mahaim fibers connecting the AV node directly to the ventricle (nodo-ventricular
fiber), bundle of His directly to ventricle (Hisioventricular fiber) and bundle branches or fascicles
directly to the ventricles (fasciculoventricular fiber). (C) A bypass tract connecting the atrium di-
rectly to the bundle of His. This is often associated with a Hisioventricular fiber resulting in a pat-
tern similar to the WPW ECG (A). (D) A small AV node resulting in a short PR interval and a normal
QRS complex. ECG, electrocardiogram; WPW, Wolff-Parkinson-White.
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286 Chapter 20
n Hisioventricular connection: A bypass tract
connecting the His bundle directly to the ventri-
cle (Fig. 20.28B,C).
n Fasciculoventricular connection: A bypass tract
connecting the right bundle, left bundle, or fasci-
cles directly to the ventricles (Fig. 20.28B)
n Atrio-Hisian connection: Connects the atria di-
rectly to the His bundle, thus bypassing the AV
node (Fig. 20.28C).
Superconducting AV node: Small AV node result-
ing in a short PR interval with normal QRS complex
(Fig. 20.28D).
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Wellens HJJ. Wolff-Parkinson-White syndrome Part I. Diagno-
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Ventricular Arrhythmias
Premature Ventricular Complexes
Ventricular complexes: Premature impulses origi-
nating from the ventricles that occur earlier than the
next expected normal sinus impulse are called prema-
ture ventricular complexes (PVCs) (Fig. 21.1).
PVCs are not preceded by P waves.
They are wide measuring 0.12 seconds because
they originate from the ventricles below the bifurca-
tion of the bundle of His. The impulse does not fol-
low the normal intraventricular conduction system
and is conducted from one ventricle to the other by
direct muscle cell to muscle cell transmission.
The ST segment and T waves are opposite in direc-
tion (discordant) to the QRS complex.
The QRS complex is followed by a pause that is usu-
ally fully compensatory.
PVCs are often called ventricular extrasystoles. They
occur very frequently in individuals with normal or ab-
normal hearts and are one of the most commonly en-
countered complexes in electrocardiography.
PVCs can be unifocal or multifocal.
Unifocal: Premature ventricular impulses that orig-
inate from a single location in the ventricle are uni-
focal PVCs. The PVCs are uniform and have identi-
cal configuration (Fig. 21.2).
Normally conducted
Atria sinus impulse
PVC Compensatory
pause
Ventricles
21
Multifocal: Ventricular complexes that originate
from two or more locations in the ventricle are mul-
tifocal PVCs. These PVCs have different configura-
tions (Fig. 21.3).
Interpolated PVC: The PVC is interpolated when it is
inserted between two sinus impulses without altering
the basic sinus rate. An interpolated PVC is not fol-
lowed by a pause (Fig. 21.4).
The PVC may or may not be followed by a fully com-
pensatory pause.
Fully compensatory pause: The pause after a PVC
is usually fully compensatory because the PVC does
not discharge the sinus node prematurely; thus, the
regularity of the sinus impulse is not interrupted
(Fig. 21.5). The presence of a fully compensatory
pause often differentiates a PVC from a premature
atrial complex.
Less than fully compensatory pause: The pause
after a PVC may be less than fully compensatory if
the PVC is conducted retrogradely to the atria (ven-
triculoatrial conduction; Fig. 21.6) and discharges
the sinus node prematurely. Because the sinus node
is discharged earlier, its rate is reset causing the
pause to be less than fully compensatory. The im-
pulse may often suppress the sinus node, which may
result in a much longer than fully compensatory
pause.
Figure 21.1: Premature Ventricular Com-
plex (PVC). The diagram on the left shows an
impulse (star) originating from the ventricle be-
low the bifurcation of the bundle of His. The
rhythm strip on the right shows two sinus com-
plexes followed by a wide, bizarre looking com-
plex called PVC (marked by a star). This complex
is premature occurring before the next sinus im-
pulse.The QRS deflection is wide and the ST
segment and T wave are discordant followed by
a compensatory pause.
287
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288 Chapter 21

A (1340 ms) = B (1340 ms)

Figure 21.2: Unifocal Premature Ventricular Complexes (PVCs). The two PVCs
noted in the rhythm strip, marked by stars, are identical in configuration and are unifocal in
origin. Note also that the pause following the PVC is fully compensatory, meaning that dis-
tance A, which straddles the PVC, measures the same as distance B, which straddles a
normal sinus impulse. ms, milliseconds.

Figure 21.3: Multifocal Premature Ventricular Complexes (PVCs). The PVCs marked
by the stars have different configurations and are multiformed. These PVCs originate from differ-
ent locations in the ventricles and are multifocal in origin.

A = 1200 ms = B = 1200 ms

Figure 21.4: Interpolated Premature Ventricular Complex (PVC). The PVC (star) is
interpolated if it is sandwiched between two sinus complexes and is not followed by a pause.
Note that the basic rate is not altered by the PVC (distance A, which represents the basic sinus
rate is the same as distance B, which straddles a PVC). ms, milliseconds.

A = 1360 ms B = 1360 ms

Figure 21.5: Fully Compensatory Pause. Rhythm strip shows a premature ventricular
complex (PVC) with a fully compensatory pause.The pause after a PVC is fully compensatory if
the PVC does not reset the sinus node; thus, distance A, which straddles a PVC, measures the
same as distance B, which straddles a normal sinus impulse.
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Ventricular Arrhythmias 289

Retrograde P A = 2160 ms B = 2360 ms

waves

Figure 21.6: Less Than Fully Compensatory Pause. Rhythm strip shows two prema-
ture ventricular complexes (PVCs) with retrograde conduction to the atria. When this occurs,
the PVC may reset the sinus node. Note that the distance between two sinus impulses strad-
dling a PVC (distance A) is shorter than the distance between two impulses straddling a
sinus impulse (distance B). ms, milliseconds.

Ventriculoatrial conduction: The ventricular im-
pulse may conduct retrogradely across the atrioven-
tricular (AV) node to activate the atria (Fig. 21.6). Al-
though retrograde conduction to the atria may occur
after a PVC, the retrograde P waves are not always vis-
ible because they are buried within the ST-T complex.
R on T phenomenon: This refers to an early PVC
striking the terminal portion of the T wave of the pre-
vious complex (Fig. 21.7). A PVC manifesting the R on
T phenomenon has a short coupling interval.
End-diastolic PVC: The PVC is end-diastolic if it oc-
curs very late in diastole, so late that the next sinus P
wave is already inscribed (Fig. 21.8). This usually re-
sults in a fusion complex. An end-diastolic PVC has a
long coupling interval.
Coupling interval: The coupling interval is the dis-
tance between the PVC and the preceding QRS com-
plex. The coupling interval of most PVCs is usually
constant. End-diastolic PVCs have long coupling inter-
vals because they occur very late during diastole after
the sinus P wave is inscribed (Fig. 21.8). Conversely,
PVCs manifesting the R on T phenomenon have short
coupling intervals, usually measuring 0.40 seconds.
Because the coupling interval is short, the PVCs occur
at the downslope of the T wave of the previous com-
plex (Fig. 21.7), which corresponds to the vulnerable
period of the ventricles. This may potentially trigger a
ventricular arrhythmia.
PVCs can occur as single beats but can be repetitive, oc-
curring in bigeminy, trigeminy, quadrigeminy, etc.
PVCs in bigeminy: PVCs are bigeminal if every
other complex is a PVC (Fig. 21.9).
PVCs in trigeminy: PVCs are trigeminal if every
third complex is a PVC (Fig. 21.10). It is also trigem-
inal if there are two consecutive PVCs and the third
complex is a sinus impulse (Fig. 21.11).
PVCs in quadrigeminy: The PVCs are quadrige-
minal if every fourth complex is a PVC (Fig. 21.12).
Paired PVCs: PVCs occur in pairs or in couplets
when two PVCs occur consecutively (Fig. 21.11).
PVCs may originate from the right ventricle or left ven-
tricle. The electrocardiogram (ECG) is helpful in dif-
ferentiating one from the other.
PVCs from the Right Ventricle
Right ventricular PVC: PVC that originates from the
right ventricle has a left bundle branch block (LBBB)
configuration. Right ventricular PVCs may originate
from any of the following locations (Fig. 21.13):
Right ventricular apex: The PVC has LBBB con-
figuration and the axis in the frontal plane is devi-
ated to the left (Fig. 21.14).

Coupling interval PVC Coupling interval PVC

Figure 21.7: R on T Phenomenon. The premature ventricular complexes (PVCs)

occur early, hitting the T wave of the previous complex. These PVCs have short coupling
intervals of 0.40 seconds. The down slope of the T wave corresponds to the vulnera-
ble period of the ventricle when the ventricular myocytes are in the process of repolariza-
tion. This can result in reentry within the ventricles when a stimulus like a PVC occurs.
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290 Chapter 21

Coupling End diastolic PVC

interval

Figure 21.8: End-Diastolic Premature Ventricular Complex (PVC). The PVC is

end-diastolic when it occurs very late, after the sinus P wave has been inscribed.

Figure 21.9: Premature Ventricular Complexes (PVCs) in Bigeminy. The PVCs alter-
nate with normal sinus complexes.

Figure 21.10: Premature Ventricular Complexes (PVCs) in Trigeminy. There are two
sinus complexes and the third complex is a PVC.

Figure 21.11: Trigeminy, also Ventricular Couplets or Paired Premature Ventricu-

lar Complexes (PVCs). One sinus complex and two consecutive PVCs also constitute
trigeminy. These PVCs can also be described as occurring in pairs or in couplets.

Figure 21.12: Premature Ventricular Complexes (PVCs) in Quadrigeminy. Every

fourth complex is a PVC.
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Ventricular Arrhythmias 291

V1

LBBB configuration RBBB configuration

Right Ventricle Left Ventricle

Normal
LAD RAD Axis
RAD LAD

Apex Outflow Inflow* Anterosuperior Inferoposterior

Figure 21.13: Localizing the Origin of the Premature Ventricular Complex (PVC). See
text for explanation. LAD, left axis deviation; LBBB, left bundle branch block; RAD, right axis deviation;
RBBB, right bundle branch block. *When the PVC has a normal axis, the PVC could originate from the
right ventricular inflow or the area between the right ventricular apex and right ventricular outflow.

Figure 21.14: Premature

Ventricular Complexes
(PVCs) of Right Ventricular
Origin. PVCs originating from
the right ventricular apex have
left bundle branch block (LBBB)
configuration (rS complex in V1
and tall R in V6) with left axis de-
viation.The pattern is very similar
to a pacemaker induced ventric-
ular rhythm with the endocardial
electrode positioned at the apex
of the right ventricle.

Figure 21.15: Premature

Ventricular Complexes
(PVCs) Originating from the
Right Ventricular Outflow.
The PVCs have left bundle branch
block (LBBB) configuration with
rS in V1 and tall R waves in V6.
There is right axis deviation of
the PVC in the frontal plane.
These PVCs originate below the
pulmonic valve in the right ven-
tricular outflow area.
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292 Chapter 21

Figure 21.16: Premature Ventricular Complexes (PVCs) from Right Ventricular

Inflow. PVCs from right ventricular inflow (tricuspid area) have left bundle branch block
(LBBB) configuration with rS complex in V1 and tall R in V6. The axis of the PVC is normal in the
frontal plane. This type of PVC may also originate between right ventricular apex and right
ventricular outflow.

Right ventricular outflow: The PVC has a LBBB
configuration and the axis in the frontal plane is de-
viated to the right (Fig. 21.15).
Right ventricular inflow: The PVC has LBBB con-
figuration and the axis of the PVC in the frontal
plane is normal. A PVC with this configuration can
originate from the right ventricular inflow (tricus-
pid area), although it could also originate from the
area between the right ventricular apex and right
ventricular outflow (Fig. 21.16).
Ventricular Parasystole
PVCs from the Left Ventricle
Left ventricular PVC: PVC that originates from the
left ventricle have right bundle branch block (RBBB)
configuration. Left ventricular PVCs may originate
from the anterosuperior or inferoposterior areas (Fig.
21.13):
Anterosuperior area: This area is supplied by the
left anterior fascicular branch of the left bundle
branch. The PVC has a RBBB configuration and the
axis is deviated to the right (Fig. 21.17).
Inferoposterior area: This area is supplied by the
left posterior fascicular branch of the left bundle
branch. The PVC has a RBBB configuration and the
axis is deviated to the left (Fig. 21.18).
Figure 21.14 shows PVCs originating from right ven-
tricular apex; Figure 21.15 shows PVCs originating
from the right ventricular outflow.
Parasystole: Parasystole refers to an independent ec-
topic impulse that competes with the sinus node as the
pacemaker of the heart. This ectopic impulse may be lo-
cated in the atria, AV junction, or ventricles. The most
commonly recognized location of a parasystole is in the
ventricles.
Ventricular parasystole: Regular automatic cells
from the AV junction and ventricles can not discharge
independently because they are constantly depolarized
and reset by the propagated sinus impulse. These auto-
matic cells serve as backup pacemakers and become

Figure 21.17: Premature

Ventricular Complexes
(PVCs) from Left Ventricle.
PVCs originating from the left
ventricle in the area supplied by
the left anterior fascicle have right
bundle branch block (RBBB)
configuration and right axis
deviation.
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Ventricular Arrhythmias 293

Figure 21.18: Premature Ventricular Complexes (PVCs) from the Left Ventricle.
PVCs originating from the left ventricle in the area supplied by the left posterior fascicle have
right bundle branch block (RBBB) configuration and left axis deviation.

manifest only when the sinus node fails. Parasystole is
different in that the cells are protected and cannot be
discharged or reset by the sinus impulse. The parasys-
tolic focus therefore can compete independently with
the sinus impulse for control of the ventricles. The
ventricular parasystole may or may not be able to cap-
ture the ventricles depending on the state of refrac-
toriness of the ventricles. Thus, when the ventricles are
not refractory from the previous sinus impulse, the
parasystole may be able to capture the ventricles. Sim-
ilarly, when the ventricles are still refractory from the
previous impulse, the parasystole will not be able to
capture the ventricles. Additionally, the sinus impulse
and the ventricular parasystole may be able to capture
the ventricles simultaneously resulting in fusion beats.
A premature ventricular impulse is therefore consid-
ered parasystolic when all of the following features are
present (Fig. 21.19).
The coupling intervals of the ventricular complexes
are variable.
Fusion complexes are present.
The ventricular complexes are mathematically re-
lated. Because the parasystolic focus is firing contin-
uously, the longer interectopic intervals are multi-
ples of the shorter interectopic intervals.
Classification of Ventricular
Arrhythmias
Classification of ventricular arrhythmias: Accord-
ing to the American College of Cardiology/American
Heart Association/European Society of Cardiology
(ACC/AHA/ESC) 2006 guidelines, ventricular arrhyth-
mias can be classified according to clinical presenta-
tion, ECG presentation, and disease entity.
Clinical presentation:
Hemodynamically stable
n Asymptomatic
n Minimally symptomatic (palpitations)
Hemodynamically unstable
n Presyncope (dizziness, lightheadedness, feeling
faint or graying out)
n Syncope (sudden loss of consciousness with
spontaneous recovery)

1640 ms 1640 ms 1640 ms 1640 ms

760 ms 640 ms 580 ms 460 ms

Figure 21.19: Ventricular Parasystole. The rhythm is normal sinus interrupted by ectopic ventricular complexes
with coupling intervals that vary from 460 to 760 milliseconds.The intervals between the ectopic ventricular complexes
are constant measuring 1,640 milliseconds. The first ventricular complex marked by a star is a fusion complex.The pres-
ence of variable coupling intervals, fusion complex, and the constant intervals between the ectopic ventricular
complexes suggest that the ventricular impulse is parasystolic.
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294 Chapter 21

Figure 21.20: Ventricular Parasystole. The rhythm is normal sinus. Parasystolic impulses compete with the
sinus rhythm resulting in ventricular complexes (arrows) with variable coupling intervals (dotted brackets). Fusion
complexes (marked by stars) are also present. The last parasystolic impulse occurred during the refractory period of
the ventricles and was not captured (last arrow).

n Sudden cardiac death (death from unexpected

circulatory arrest occurring within an hour after
onset of symptoms).
n Sudden cardiac arrest (death from unexpected
circulatory arrest usually from cardiac arrhyth-
mia occurring within an hour after onset of
symptoms in which medical intervention such as
defibrillation reverses the event).
Electrocardiographic presentation:
Nonsustained ventricular tachycardia (VT)
n Monomorphic (Fig. 21.21)
n Polymorphic
Sustained VT
n Monomorphic (Fig. 21.22)
n Polymorphic
Bundle branch reentrant tachycardia
Bidirectional VT (Fig. 21.23)
Torsades de pointes (Figs. 21.24 to 21.29)
Ventricular flutter (Fig. 21.30)
Ventricular fibrillation (Fig. 21.31)
Disease entity: The clinical and disease entities in
which ventricular arrhythmias may occur include
coronary disease, heart failure, congenital heart dis-
ease, neurological disorders, structurally normal
hearts, sudden infant death syndrome, and cardiomy-
opathies (dilated, hypertrophic, and arrhythmogenic
right ventricular cardiomyopathy).
Ventricular Tachycardia
VT: Three PVCs in a row is a triplet. Three or more con-
secutive PVCs with a rate that exceeds 100 beats per
minute (bpm) is VT. VT can be classified as sustained
or nonsustained, monomorphic or polymorphic.
Nonsustained VT: VT is nonsustained if the tachy-
cardia terminates spontaneously within 30 seconds
(Fig. 21.21).
Sustained VT: VT is sustained if the tachycardia
lasts more than 30 seconds (Fig. 21.22). It is also
sustained if the tachycardia is associated with hemo-
dynamic compromise, such as dizziness, hypoten-
sion, or near syncope, even if the duration of the VT
is 30 seconds.
Monomorphic VT: VT is monomorphic if the ven-
tricular complexes have a single or uniform config-
uration and may be nonsustained (Fig. 21.21) or
sustained (Fig. 21.22).
Polymorphic VT: VT is polymorphic if the QRS
complexes are multiformed or have different config-
urations and may be nonsustained (Fig. 21.24) or
sustained (Fig. 21.25 and Figs. 21.27-21.28).
Bundle branch reentrant tachycardia: This type of
VT is due to reentry. The pathway usually involves the left
bundle branch, bundle of His, right bundle branch, ven-
tricular septum, and back to the left bundle branch and

Figure 21.21: Nonsustained Monomorphic Ventricular Tachycardia (VT). Three or

more consecutive premature ventricular complexes (PVCs) with a rate of 100 complexes per
minute is VT. The VT is monomorphic because the ventricular complexes have the same configu-
ration. The VT is nonsustained because the duration of the tachycardia is 30 seconds.
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Figure 21.22: Sustained Monomorphic Ventricular Tachycardia (VT). The VT is

monomorphic because the QRS complexes are uniform. VT is sustained if the duration is
30 seconds or the tachycardia is associated with hemodynamic symptoms of hypotension,
dizziness or near syncope even if the tachycardia terminates spontaneously within 30 seconds.

Figure 21.23: Bidirectional Ventricular Tachycardia. The QRS complexes have right
bundle branch block (RBBB) configuration with tall R waves in V1. The axis of the QRS complex in
the frontal leads alternates from left axis to right axis indicating that the origin of the tachycardia
alternates between left anterior and left posterior fascicles.

Figure 21.24: Polymorphic Ventricular Tachycardia (PVT). Twelve-lead electrocardiogram showing non-
sustained PVT. The rate of the PVT is very rapid and irregular and the QRS complexes have varying morphologies.
The QTc is 0.46 seconds and is prolonged. When the QTc is prolonged, the PVT is called torsades de pointes. Lead II
rhythm strips are recorded at the bottom of the tracing.

295
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A.

B.

Figure 21.25: Polymorphic Ventricular Tachycardia (PVT). (A) Twelve-lead electrocardiogram (ECG)
showing PVT.The QRS complexes have different sizes and shapes and the rate is very rapid and irregular at almost
300 beats per minute. (B) The ECG immediately after successful cardioversion showed acute inferior myocardial in-
farction with a QTc of 0.44 seconds.

Figure 21.26: Torsades de A.

Pointes. Electrocardiogram (ECG)
(A): Baseline 12-lead ECG showing
unusually prolonged QTc of 0.70
seconds. Rhythm strip (B) is from the
same patient showing nonsustained
torsades de pointes. There are
pauses (long cycles) on termination
of the tachycardia. These pauses
prolong the QT interval of the next
complex. The compensatory pauses
of single PVCs also result in long cy-
cles, which also prolong the QTc of B. Long cycle Short cycle
the next complex and facilitates the
onset of torsades de pointes.

296
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Ventricular Arrhythmias 297

Figure 21.27: Torsades de Pointes. The classical pattern of torsades de pointes is seen in
the rhythm strip. The polarity of the QRS complexes keeps changing. Some QRS complexes seem
to point up and others down. An isoelectric zone is marked by the arrow, which represents the
node. The taller complexes represent the spindle.

Figure 21.28: Polymorphic Ventricular Tachycardia. The ventricular tachycardia starts

with the fourth complex and continues to the end of the rhythm strip. Note that the rate of the
tachycardia is unusually rapid and the ventricular complexes are polymorphic with some com-
plexes pointing downward and other complexes pointing upward as shown by the arrows.

Figure 21.29: Polymorphic

Ventricular Tachycardia
(PVT). Continuous rhythm strip
showing sustained PVT deterio-
rating to ventricular fibrillation
terminated by DC shock of 200
joules. The small arrow at the
second rhythm strip is a precor-
dial thump that was not success-
ful in terminating the tachycar-
dia. The QTc is not prolonged.
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298 Chapter 21

Figure 21.30: Ventricular Flutter. The QRS complexes are wide and uniform with a rate of
approximately 300 beats per minute. The QRS complexes are monomorphic and there are no iso-
electric intervals between the QRS complexes.Ventricular flutter is similar to monomorphic ven-
tricular tachycardia (VT) except for the higher heart rate and has the same clinical significance.

left ventricle. During tachycardia, the right ventricle is
activated anterogradely through the right bundle branch
and the left ventricle through the ventricular septum.
Thus, the QRS complexes are wide measuring 0.14 sec-
onds with a LBBB pattern. During normal sinus rhythm,
the baseline ECG usually shows evidence of His-Purkinje
system disease with complete or incomplete LBBB often
with a slightly prolonged PR interval. This type of VT
should be identified because if sustained and recurrent,
the VT may respond to radiofrequency ablation.
Bidirectional tachycardia: In bidirectional tachycardia,
the VT originates from two separate locations, the left an-
terior and left posterior fascicles of the left ventricle. Thus,
the VT has RBBB configuration and the axis of the ectopic
Torsades de Pointes
impulse alternates between right and left axis in the
frontal plane (Fig. 21.23). When the ectopic impulse orig-
inates from the left anterior fascicle, the QRS complex is
deviated to the right. When the ectopic impulse originates
from the left posterior fascicle, the QRS complex is devi-
ated to the left (see origin of PVCs, Fig. 21.13). This type
of VT is frequently associated with digitalis toxicity.
Polymorphic Ventricular Tachycardia
Polymorphic VT: Polymorphic VT or PVT refers to a
wide complex tachycardia with varying morphology of
the QRS complexes (Fig. 21.24). The tachycardia is very
unique in that the QRS complexes keep changing in
size, shape, and direction. The rate of the tachycardia is
usually rapid and irregular causing the patient to be-
come hemodynamically unstable even when the VT is
only of short duration. The configuration of the QRS
complex may fluctuate and appear upright and then
twists itself to become inverted with an isoelectric tran-
sition point, thus resembling a spindle and node. The
PVT may occur in short bursts and may be self-termi-
nating. If the arrhythmia becomes sustained (30 sec-
onds), the tachycardia may degenerate to ventricular
fibrillation and can cause sudden death.
Torsades de pointes: PVT may or may not be associ-
ated with prolonged QT interval. When the PVT is as-
sociated with prolonged QT interval, the VT is called
torsades de pointes. When the PVT is associated with
normal QT interval, the VT is a regular form of PVT.
Torsades de pointes should be differentiated from reg-
ular PVT because the treatment of torsades de pointes
is different from that of regular PVT.
Regular PVT: The 12-lead ECG of a patient with sus-
tained PVT is shown (Fig. 21.25A). The 12-lead ECG
immediately after she was successfully cardioverted to
normal sinus rhythm showed acute inferior myocardial
infarction (Fig. 21.25B) with normal QTc of 0.44
seconds.

Figure 21.31: Ventricular Fibrillation. In ventricular fibrillation, the rhythm is very dis-
organized and ineffective with an undulating baseline. The QRS complexes are very irregular
and are not well defined. This rhythm is fatal unless the patient is successfully resuscitated.
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Torsades de pointes: The presence of prolonged QTc
differentiates torsades de pointes from regular PVT.
The QT interval is measured during normal sinus
rhythm before or immediately on termination of the
tachycardia. The QT interval should be corrected for
heart rate because the QT interval measures longer
with slower heart rates and shorter with faster heart
rates. The QT interval corrected for heart rate is the
QTc. The QTc is prolonged when it measures 0.44
seconds in men and 0.46 seconds in women and in
children. Prolonged QTc should always be recognized
because it predisposes to torsades de pointes even
among patients without cardiac disease, which can be
fatal. The step by step calculation of the QTc is shown
in Chapter 2, Basic Electrocardiography.
Prolongation of the QTc may be inherited or it may be
acquired.
Inherited prolongation of the QTc: These pa-
tients are usually young and have family history of
sudden death, often occurring at a young age. In
some patients with congenitally prolonged QTc, the
QTc does not stay prolonged, but may vary. Thus,
screening of asymptomatic patients with family his-
tory of prolonged QTc may not show QT prolonga-
tion in the initial ECG examination. Additionally,
about a third of patients who are known carriers of
long QT syndrome confirmed by genetic testing will
not show QTc prolongation. The duration of the
QTc parallels the risk of developing torsades de
pointes and sudden death. A long QTc of 0.50 sec-
onds in patients with congenitally prolonged QT
syndrome is a marker of increased cardiovascular
risk. Because the QT duration exhibits marked vari-
ability, the longest QTc measured at any time during
follow-up of a patient with congenital long QT syn-
drome provides important prognostic information.
Acquired prolongation of the QTc: In normal in-
dividuals, QTc prolongation can occur during acute
myocardial ischemia, electrolyte abnormalities (hy-
pokalemia, hypocalcemia, and hypomagnesemia),
use of antiarrhythmic agents (Class IA and Class
III), antihistaminics, antifungals, antimicrobials, tri-
cyclic antidepressants, and nutritional causes result-
ing from alcohol, liquid protein diet, anorexia, and
starvation. A long list of agents that can cause pro-
longed QTc can be accessed through Web sites at
www.torsades.org or www.qtdrugs.org.
During tachycardia, the QRS complexes of torsades de
pointes and regular PVT are similar and are both poly-
morphic. During normal sinus rhythm, the QTc of tor-
sades de pointes is prolonged, whereas the QTc of reg-
ular PVT is not. Torsades de pointes is pause
dependent, occurring when there is bradycardia, which
is known to prolong the QTc. The arrhythmia is fre-
quently seen in the setting of long/short cycles as
shown in Figure 21.26B.
Ventricular Arrhythmias 299
PVT with or without prolongation of the QTc is a serious
arrhythmia that can become sustained and can cause
sudden death. Even when the tachycardia is short and
self-terminating, it is associated with symptoms and is
usually not tolerable because of the very rapid ventricular
rate as shown in the examples (Figs. 21.28 and 21.29).
Ventricular flutter: Ventricular flutter is similar to
monomorphic VT except for a higher heart rate of ap-
proximately 300 bpm. There is no isoelectric interval
between the QRS complexes. Because of the unusually
rapid ventricular rate, the arrhythmia is seldom toler-
ated (Fig. 21.30). Ventricular flutter and VT are treated
similarly.
Ventricular fibrillation: Ventricular fibrillation is a
disorganized ventricular rhythm with poorly defined
QRS complexes. The baseline is undulating and the
QRS complexes are very irregular with varying sizes and
shapes (Fig. 21.31). Monomorphic and polymorphic
VT and ventricular fibrillation are frequently seen in
patients with cardiac disease and severe left ventricular
dysfunction. It can also occur in patients with struc-
turally normal hearts such as patients with prolonged
QT syndrome or patients with the Brugada syndrome.
Figure 21.32 summarizes diagrammatically the differ-
ent ventricular arrhythmias.
Summary of ECG Findings
1. A PVC is a premature complex that is wide with an ST segment
and T wave that are opposite in direction to the QRS complex.
This is followed by a pause that is fully compensatory. PVCs
are often called ventricular extrasystoles with coupling inter-
vals that are fixed.
2. A ventricular parasystole is a ventricular ectopic impulse that is
protected. It is identified by the presence of fusion complexes,
variable coupling intervals, and longer interectopic intervals that
are mathematically related to the shorter interectopic intervals.
3. VT is present when three or more PVCs occur consecutively
with a rate 100 bpm. VT can be sustained or nonsustained,
monomorphic, or polymorphic.
The VT is nonsustained if the duration of the tachycardia
is 30 seconds.
The VT is sustained if the duration is 30 seconds or if the
tachycardia is associated with hemodynamic symptoms
such as hypotension, dizziness, or syncope even if the tachy-
cardia is self-terminating with a duration of 30 seconds.
VT is monomorphic if the QRS complexes are uniform in
configuration.
VT is polymorphic if the QRS complexes have varying
morphologies.
Torsades de pointes is a special form of polymorphic
VT associated with prolonged QTc.
Regular polymorphic VT is similar to torsades de pointes
except that the baseline QT interval is not prolonged.
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300 Chapter 21

Summary of the Different Types of Ventricular Complexes

Interpolated
PVC

PVCs in
Bigeminy

PVCs in
Trigeminy

Multifocal PVCs
also in Bigeminy

Paired or Back
to Back PVCs

Nonsustained
monomorphic
VT

Nonsustained
Polymorphic
VT

Ventricular
Fibrillation

Figure 21.32: Ventricular Arrhythmias. Diagram shows examples of different ventricular

arrhythmias. Arrows point to the ventricular ectopic complexes.

4. Ventricular flutter has monomorphic ventricular complexes
with a rate of approximately 250 bpm. The QRS complexes
are not separated by isoelectric intervals.
5. Ventricular fibrillation has very disorganized rhythm with
poorly defined QRS complexes with a rate of 300 bpm and is
fatal if not emergently cardioverted.
Mechanism
PVCs look different from normally conducted sinus im-
pulses because PVCs originate from the ventricles below the
bifurcation of the bundle of His. The impulse activates the
ventricles sequentially by spreading from one ventricle to
the other. This is in contrast to a supraventricular impulse,
which originates above the bifurcation of the bundle of His,
resulting in activation of both ventricles synchronously
causing the QRS complexes to be narrow.
PVCs are commonly extrasystolic and are usually related to
the preceding impulse most probably because of reentry of
the impulse within the ventricles. Thus, the coupling inter-
vals of extrasystoles are constant or fixed.
A ventricular parasystole is an independent pacemaker that
is protected and is not depolarized by the propagated sinus
impulse. It can therefore compete with the sinus node inde-
pendently for control of the ventricles. Unlike ventricular
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extrasystoles, it bears no relationship to the preceding ven-
tricular complex; thus, the coupling interval is not fixed. The
impulse can capture the ventricles only when the ventricles
are not refractory from the previous sinus impulse. Fusion
beats are therefore present and the intervals between parasys-
tolic impulses are mathematically related.
The origin of the ventricular impulse can be predicted by ex-
amining the morphology of the QRS complex in the 12-lead
ECG. Briefly, ectopic ventricular complexes originating from
the left ventricle will show positive or tall R waves in V1
(RBBB pattern) because the impulse has to travel from left
ventricle to right ventricle toward lead V1. Ventricular com-
plexes originating from the right ventricle will show negative
or deep S waves in V1 (LBBB pattern) because the impulse has
to travel from right ventricle to left ventricle away from V1.
VT both sustained and nonsustained may be due to en-
hanced automaticity of cells within the myocardium or His-
Purkinje system. It could also be due to triggered activity, as
in digitalis toxicity. It can also be due to reentry requiring the
presence of two separate pathways with different electro-
physiologic properties within the ventricles.
Repolarization of the millions of individual myocardial cells in
the ventricles is not homogeneous because there are intrinsic
differences in the action potential duration among the various
cells composing the myocardium. This inhomogeneity or dis-
persion in ventricular repolarization will cause some cells to
become excitable, whereas others continue to be refractory.
This period may be extended when phase 3 is delayed or when
there is prolongation of the action potential duration and QT
interval. An ectopic impulse presented to the ventricles during
this vulnerable period, which corresponds to the mid and ter-
minal portion of phase 3 of the action potential, represented
by the downslope of the T wave in the ECG (R on T phenom-
enon) may cause a reentrant tachycardia within the ventricles.
Thus, QT dispersion 100 milliseconds, representing the dif-
ference between the longest and shortest QT interval in the 12-
lead ECG, may be helpful in predicting those who are high risk
for ventricular arrhythmias.
When acute myocardial ischemia and injury are present, the
triggering impulse may not have to occur during the vulnerable
phase of ventricular repolarization to cause ventricular arrhyth-
mias because the presence of injured myocardium can further
increase QT dispersion. Thus, in the setting of acute myocardial
infarction, early and late PVCs are as likely to trigger VT.
Clinical Significance
Simple PVCs: Single and frequent PVCs including multi-
formed complexes are commonly seen in patients with car-
diac disease, although they are also present in healthy individ-
uals with structurally normal hearts. In normal individuals,
the frequency of ectopic ventricular complexes increases with
increasing age.
During infancy: PVCs are rare during infancy. In a 24-
hour Holter study of 134 healthy, full-term newborn in-
fants, 19 had premature complexes, all supraventricular.
Ventricular Arrhythmias 301
During childhood: Among healthy children, ages 7 to 11
years, 24-hour Holter monitor showed premature com-
plexes only in 20 of 92 children. The premature com-
plexes were supraventricular in 19 children and only 1
had a PVC.
Medical students: Among 50 healthy male medical stu-
dents, 24-hour Holter study showed isolated PVCs in 25
(50%) and were multifocal in 6 (12%). One (2%) had
couplets and another (2%) had nonsustained VT defined
as three or more PVCs in a row with a rate 100 bpm.
Elderly population: Among 98 healthy elderly patients
aged 60 to 85, 78 (80%) had ventricular arrhythmias. Ven-
tricular couplets were present in 11 (11%) and nonsustained
VT in 4 (4%). Multiformed PVCs were present in 34 (35%),
12 (12%) had 30 PVCs any hour, 7 (7%) have 60 PVCs
any hour, and 17 (17%) had total of 100 PVCs in 24 hours.
Frequent and complex PVCs: Complex PVCs consisting of
frequent multiformed ventricular complexes and nonsus-
tained monomorphic VT are generally benign in completely
asymptomatic individuals if there is no demonstrable car-
diac disease and left ventricular systolic function is pre-
served. However, in patients with structural cardiac diseases,
especially those with left ventricular dysfunction, these ven-
tricular arrhythmias need further evaluation.
Healthy population: Long-term follow-up (3 to 9.5 years,
mean 6.5 years) of 73 asymptomatic and healthy individu-
als, age 18 to 72 years, with frequent complex ventricular
ectopy including those with nonsustained VT by 24-hour
Holter (mean PVCs per hour 566, multiformed PVCs 63%,
ventricular couplets 60%, nonsustained VT 26%), showed
no increased mortality and a long-term prognosis similar
to that of the general healthy population.
Patients with left ventricular dysfunction: Although
these ventricular arrhythmias are not targets for pharma-
cologic therapy in the hospital or outpatient setting, pa-
tients with left ventricular dysfunction (ejection fraction
of 40%) with frequent and complex ventricular ectopy
should be referred for further evaluation because they
may be at risk for more serious arrhythmias.
Ventricular parasystole: Ventricular arrhythmias that are
known to be parasystolic are considered benign and require
no therapy. A ventricular parasystole should always be sus-
pected when the coupling intervals of the PVCs are not fixed.
They are also recognized by fusion beats and the intervals be-
tween complexes are mathematically related.
Sustained VT and ventricular fibrillation: Sustained VT
and ventricular fibrillation are malignant arrhythmias that
can cause sudden death. They commonly occur as a compli-
cation of acute myocardial infarction. They are also seen in
patients with structural cardiac diseases especially ischemic,
nonischemic, and hypertrophic cardiomyopathies. It is rare
in patients with structurally normal hearts unless there is:
Long QT syndrome, acquired or congenital
Brugada syndrome
Wolff-Parkinson-White syndrome
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302 Chapter 21
The long QT syndrome: The QT interval is prolonged when
the QTc measures 0.44 seconds (or 440 milliseconds) in
men and 0.46 seconds (or 460 milliseconds) in women.
A long QT interval predisposes to torsades de pointes, which
is a special type of polymorphic VT. The following is a sim-
plified review of the ionic changes that occur in the ventricu-
lar myocyte that can result in prolongation of the QT inter-
val (see Chapter 1, Basic Anatomy and Electrophysiology).
Mechanism of the prolongation of the QT interval:
During depolarization or phase 0 of the action potential,
the fast sodium channels open briefly allowing sodium ions
to enter the cell. The entry of positive ions into the cell
causes the polarity of the cell to change abruptly from 90
to 10 to 20 mV. Depolarization is immediately followed
by repolarization consisting of phases 1 through 3 of the
action potential. This corresponds to the J point extending
to the end of the T wave in the surface ECG. During phase
2, which corresponds to the plateau phase of the action po-
tential, the polarity of the cell is maintained at approxi-
mately 0 mV for a sustained duration. This is due to entry
of calcium into the cell because of activation of the slow or
L-type calcium channels during depolarization. This
slow but sustained flow of positive ions into the cell is
counterbalanced by the flow of potassium out of the cell
because the cell membrane is more permeable to potas-
sium than other ions. This loss of potassium makes the in-
side of the cell more negative as positive ions are lost. Thus,
the entry of calcium into the cell (entry of positive ions)
combined with flow of potassium out of the cell (loss of
positive ions) results in an equilibrium that is sustained for
a prolonged duration corresponding to the plateau or
phase 2 of the action potential. When the calcium channels
are inactivated, the entry of calcium into the cell is sud-
denly prevented although the outward flow of potassium
continues. This inequity in calcium entry and potassium
outflow advances the action potential to phase 3. Phase 3 or
rapid repolarization is due to continuous efflux of potas-
sium from the cell causing the cell to become more negative
until the resting potential of 90 mV is reached. This marks
the end of phase 3 of the action potential, which corre-
sponds to the end of the T wave in the surface ECG.
As long as the potential of the ventricular myocyte is pre-
vented from reaching 90 mV, which is the normal resting
potential, the cell is not fully repolarized. Thus, any mech-
anism that will prolong or increase the entry of sodium or
calcium into the cell will make the inside of the cell more
positive and will delay or prolong the duration of the ac-
tion potential. Similarly, any mechanism that will inhibit
or delay the exit of potassium out of the cell will make the
cell less negative. This will also prolong the duration of
the action potential.
Phases 0 through 3 of the transmembrane action poten-
tial correspond to the duration of the action potential of
individual myocardial cells. This is equivalent to the QT
interval in the surface ECG. Prolongation of phases
1 through 3 will result in prolongation of the QT interval.
Causes of prolonged QT interval: Prolongation of the
QT interval may be acquired or it may be congenital.
n Acquired long QT: In normal individuals with normal
QTc, several pharmacologic agents can prolong the QT
interval. These include type IA antiarrhythmic agents
(quinidine, disopyramide, and procainamide), type III
antiarrhythmic drugs (dofetilide, ibutilide, sotalol, and
amiodarone), antipsychotic agents (chlorpromazine,
thioridazine, and haloperidol), macrolide antibiotics
(erythromycin, clarithromycin), antifungal agents (ket-
onazole and itraconazole), electrolyte disturbances no-
tably hypomagnesemia and hypokalemia, and other
agents such as pentamidine and methadone. A long list
of pharmacologic agents that can prolong the QT in-
terval can be accessed at www.torsades.org. Although
the use of a single pharmacologic agent (quinidine or
ibutilide) may cause QT prolongation and torsades de
pointes almost immediately, occasionally, a combina-
tion of two agents may be needed to prolong the QT
interval such as the concurrent use of erythromycin
and ketonazole. Erythromycin, a macrolide antibiotic,
and ketonazole, an antifungal agent, are both metabo-
lized by the liver through the cytochrome P-450 3A4
(CYP 3A4) metabolic pathway. Either agent can poten-
tially prolong the QT interval although prolongation
of the QT interval is more significant when both agents
are taken concurrently because they compete for the
same metabolic pathway resulting in increased plasma
concentration of both agents. Similarly, an agent that
does not prolong the QT interval but depends on the
CYP 3A4 metabolic pathway for clearance such as a
calcium channel blocker (verapamil) when combined
with a drug that prolongs the QT interval such as
erythromycin can result in further prolongation of the
QT interval since verapamil also depends on the same
pathway as that of erythromycin for clearance. The ef-
fect on QT prolongation and potential for torsades de
pointes may be more delayed, however.
n Congenital long QT: Congenital or inherited prolon-
gation of the QT interval affects young individuals es-
pecially the first 2 decades of life and is a common
cause of sudden death in this age group. Two types of
long QT syndrome have been clinically described.
n The first familial long QT syndrome described by
Jervell and Lange-Nielsen is associated with sen-
sorineural deafness. This type of long QT syndrome
is inherited as autosomal recessive. The second fa-
milial long QT syndrome is the Romano-Ward syn-
drome and is inherited as autosomal dominant but
is not associated with congenital deafness.
n With the advent of genetic testing, seven long QT
syndromes have been described thus far and are la-
beled LQT1 to LQT7 according to the sequence in
which the abnormal locus of the genetic defect
have been discovered. The first three entities
LQT1, LQT2, and LQT3are the most common
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and comprise almost 95% of all identified cases of
congenital long QT syndromes. The prolongation
of the QT is due to a genetic defect involving the
potassium channel in most cases except LQT3 and
LQT4, which are due to a defect in sodium trans-
port. The genetic abnormality involves the ion
channel in almost all cases except LQT4, which
does not affect the ion channel directly, but only its
supporting structure.
n Patients with long QT syndrome can be confirmed
by genetic testing, although a negative genetic test
will not exclude the presence of congenital long
QT syndrome because up to 40% of patients with
congenital long QT have not been linked to any ge-
netic abnormality. Additionally, the use of genetic
testing remains very expensive and may not be af-
fordable when screening several family members
with history of long QT syndrome or known sud-
den death in the family. It also takes several weeks
before the results are known. Thus, the diagnosis
of long QT syndrome is more commonly based on
phenotypic ECG abnormalities.
n When the ECG is used in the diagnosis of patients
with congenital long QT syndrome, marked vari-
ability in the duration of the QTc in serial ECGs
can occur. Even in normal individuals, the QT in-
terval can vary by as much as 50 to 75 milliseconds
over a 24-hour period. Thus, screening of individ-
uals with family history of long QT syndrome and
sudden death may not show any initial QT prolon-
gation. Additionally, almost a third of patients who
are confirmed carriers have normal or borderline
QTc of 0.40 to 0.46 seconds. The longest QTc, in-
cluding those measured before age 10 years, pro-
vides important prognostic information during
adolescence in patients with congenital long QT
syndrome. Thus, a long QTc measuring 0.50 sec-
onds identifies a patient who has increased risk of
cardiovascular events and shorter QT intervals of
0.50 seconds decreases the risk of cardiovascular
events. In these patients, however, there is no clear
cut QT interval that is considered safe because QTc
of 0.46 seconds are also at risk for syncope and
sudden death.
n The following is a summary of the known long QT
syndromes:
LQT1: Long QT1 is the first mutation to be identified. It
is one of the most common, accounting for approxi-
mately 50% of known long QT abnormalities. The ab-
normality involves the short arm of chromosome 11.
The gene was identified using cloning techniques and
was named KvLQT1 because it encodes a potassium
channel, but was eventually renamed KCNQ1. Homozy-
gous mutation of the gene causes the Jervell and Lange-
Nielsen syndrome. The syndrome is associated with
congenital deafness, which is also due to the abnormality
Ventricular Arrhythmias 303
in the same potassium channels involved with the pro-
duction of potassium-rich endolymph in the inner ear.
It is a much more common cause of sudden death
younger than age 10 years when compared with the
other long QT syndromes. Prolongation of the QT is due
to delay in phase 3 of the action potential because of de-
lay in the transport of potassium (-subunit of the slow
potassium rectifier or IKs). In addition to the prolonged
QT, the T wave in the ECG has a slow indistinct onset,
but is otherwise normal. Patients with LQT1 are most
symptomatic during exertion because the QT interval
becomes longer with exercise in contrast to patients with
LQT3 who are most symptomatic during rest or sleep.
The QT interval can be prolonged by intravenous injec-
tion of epinephrine. Thus, in symptomatic individuals,
if the initial QT is not prolonged, the long QT can be un-
masked with epinephrine.
LQT2: Long QT2 is also one of the most common long
QT abnormalities with up to 40% of all congenital cases
of long QT syndrome. The defect resides in chromosome
7 and the identified gene is called HERG (human ether a-
go-go related gene) or KCNH2. Similar to LQT1, this gene
is also involved with the potassium current. Unlike LQT1
that affects the slow potassium currents (called slow K
rectifier or IKs), the gene is involved with the fast potas-
sium currents (called rapid K rectifier or IKr), which is
the most important in determining the duration of the
action potential. Most pharmacologic agents that prolong
the QT interval also inhibit the same potassium channel.
In LQT2, the shape of the T wave in the ECG is bifid or
split. Mutation of the HERG gene causes another abnor-
mality characterized by an unusually short QT interval of
0.30 seconds called congenital short QT syndrome,
which is also associated with sudden death.
LQT3: Unlike LQT1 and LQT2, which are involved with
potassium transport, LQT3 involves mutation of the gene
encoding a sodium channel. The abnormality is located in
chromosome 3 and the gene is called SCN5A. LQT3 is less
common than the first two long QT syndromes. The ab-
normality in the sodium channel causes prolongation of
phase 2 of the action potential. This is due to delayed clo-
sure of the fast sodium channels on completion of rapid
depolarization resulting in continuous entry of sodium
ions into the cell, thus prolonging the duration of the ac-
tion potential. The baseline ECG will show asymmetric T
waves with a steep downslope. Most patients are sympto-
matic at rest or sleep, which causes the QT interval to pro-
long because of bradycardia. Mutation of the gene
SCN5A has been implicated as the cause of the Brugada
syndrome, where most of the arrhythmic events occur
during sleep (see Brugada Syndrome).
LQT4: Long QT4 is the only other long QT syndrome asso-
ciated with abnormality in sodium transport. It is the only
long QT syndrome that is not a channelopathy because
the abnormality does not directly involve an ion channel
but its supporting structure. The abnormality resides in
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304 Chapter 21
chromosome 4 and the gene is called ankyrin-B. The ab-
normality affects the sinus node and the clinical manifesta-
tions include symptoms of sinus node dysfunction. This is
manifested as bradyarrhythmias as well as tachyarrhyth-
mias including the tachycardia bradycardia syndrome.
LQT5: This abnormality involves mutation of gene
KCNE1 in chromosome 21. The gene is also called minK.
This type of long QT syndrome is rare. Homozygous mu-
tation of this gene can also cause the Jervell and Lange-
Nielsen syndrome. The abnormality involves the trans-
port of potassium ( -subunit of the slow K rectifier or
IKs) similar to LQT1. Prolongation of the action potential
is due to delay in phase 3. The surface ECG usually shows
T wave with a wide base.
LQT6: The abnormality also resides in chromosome 21 and
involves the KCNE2 gene. This type of long QT syndrome
is rare. The abnormality affects the rapid outward potas-
sium transport (outward rapid K rectifier or IKr) resulting
in decreased potassium efflux with prolongation of phase 3
of the action potential. The T wave has low amplitude.
LQT7: The abnormality resides in chromosome 17 and the
gene involved is called KCNJ2. This abnormality prolongs
the action potential duration through its effect on the in-
ward rectifying currents involved with potassium trans-
port, thus delaying phase 3. Both cardiac and skeletal mus-
cle cells can be affected resulting in prolongation of the QT
and hypokalemia induced periodic paralysis with a large U
wave looking component in the ECG. This disorder is very
rare and is often referred to as the Andersen syndrome.
Timothy syndrome often identified as LQT8: Timothy
syndrome involves mutation of the L-type calcium channel.
The defect involves chromosome 12 and the identified gene
is CACNA1C. Calcium channel dysfunction causes multi-
system involvement with osseous deformities including
dysmorphic features and syndactyly in addition to autism,
cognitive defects, and malignant ventricular arrhythmias.
This very rare syndrome has also been referred to as LQT8.
Brugada syndrome: Another example in which malignant
ventricular arrhythmias can occur in individuals with struc-
turally normal hearts is the Brugada syndrome. Patients with
this syndrome can be identified by the presence of a peculiar
electrocardiographic pattern in baseline ECG characterized by
RBBB with rSR
configuration confined to V1 to V3. In V1 or has an implanted automatic defibrillator. Only an im-
V2, the J point and ST segment are elevated with a coved or up-
ward convexity terminating into an inverted T wave (type I). In
some patients, the elevated ST segment may assume a saddle
back configuration (type II) or often a triangular pattern in-
stead of a coved appearance (type III). Types II and III termi-
nate in upright T waves. The ST elevation is confined to the
right-sided precordial leads and is not accompanied by recip-
rocal ST depression. It may be permanent in some individuals,
although, in others, it may vary from time to time. When these
ECG changes are not present, the ST segment abnormalities
can be unmasked by administration of sodium channel blocker
such as procainamide, flecainide, or ajmaline. The QTc is not
prolonged. Examples of the Brugada ECG are shown in Chap-
ter 23, Acute Coronary Syndrome: ST Elevation Myocardial In-
farction, differential diagnosis of ST segment elevation. Ap-
proximately 90% of patients with the Brugada ECG are males.
Mechanism: The abnormality has been identified to be a
mutation in chromosome 3 involving gene SCN5A. Only
the epicardial cells of the right ventricle are affected.
These epicardial cells have abnormal sodium channels,
which causes premature repolarization. The premature
repolarization causes shortening of the duration of the
action potential only of the abnormal cells. Repolariza-
tion of normal endocardial cells is not affected. The
shortened duration of repolarization of the epicardial
cells will cause these cells to repolarize earlier when com-
pared with endocardial cells. Thus, during repolarization,
a gradient between the abnormal epicardial and the nor-
mally repolarizing endocardial cells is created during
phase 2 of the action potential resulting in elevation of
the ST segment, only in the right precordial leads V1 to V3.
This difference in repolarization between normal and ab-
normal cells can facilitate a reentrant arrhythmia.
This syndrome is a genetic defect without associated
structural cardiac disease and can cause sudden death
from polymorphic VT. Thus, the syndrome is primarily
an electrical abnormality because it has no other clinical
manifestations other than the ventricular arrhythmia.
This clinical entity is endemic in Southeast Asia including
Thailand, Japan, and the Philippines and affects mostly
males in their mid to late 30s. The ECG abnormalities as
well as the ventricular arrhythmias are enhanced by vagal
activity; thus, the ventricular arrhythmias are commonly
manifested during sleep. Because of its nocturnal
frequency, it is often called sudden unexpected nocturnal
death syndrome or SUNDS. Fever has also been shown to
be a predisposing factor. The syndrome is inherited as au-
tosomal dominant with variable expression similar to ar-
rhythmogenic right ventricular cardiomyopathy.
In patients with the Brugada ECG who are symptomatic
with syncope because of polymorphic VT or ventricular fib-
rillation, mortality is high. The incidence of VT and fibrilla-
tion is similar whether the patient is on a beta blocker, tak-
ing an antiarrhythmic agent (amiodarone) or the patient
planted defibrillator is effective in preventing sudden death
and therefore the only known effective therapy in reducing
mortality. According to the ACC/AHA/ESC 2006 guidelines
on ventricular arrhythmias, the implantable defibrillator re-
ceives Class I recommendation in patients with previous
cardiac arrest and Class IIa recommendation in patients
with history of syncope or documented VT. There are only
few agents that are useful during an arrhythmic event. This
includes isoproterenol, which receives a Class IIa recom-
mendation and quinidine, a Class IIb recommendation.
Although symptomatic patients with the Brugada ECG
are high risk for sudden death, the significance of the
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Brugada ECG in the general asymptomatic population is
uncertain because not all patients with the Brugada ECG
will develop VT or ventricular fibrillation.
n Among 63 patients with the Brugada ECG reported by
Brugada et al. in 1998, 41 were diagnosed after resus-
citated cardiac arrest or syncope and 22 were asymp-
tomatic, detected incidentally because of family his-
tory of sudden death. Of the 22 asymptomatic
individuals, 6 (27%) developed ventricular arrhyth-
mias during a mean follow-up of 27 months, whereas
among the 41 symptomatic patients, 14 (34%) had a
recurrence of the ventricular arrhythmia during a
mean follow-up of 37 months. They concluded that
asymptomatic patients with the Brugada ECG have
the same risk of developing a cardiac arrhythmia
when compared with patients who had previous his-
tory of aborted sudden death.
n However, among 32 cases with the Brugada ECG de-
tected in a population-based study of 4,788 asympto-
matic Japanese individuals younger than 50 years of
age who had biennial examinations and were followed
for 41 years, there were 7 (26%) unexpected deaths in
patients with the Brugada ECG compared with 20
(74%) in the control group. In most cases, the ECG
finding was intermittent and was nine times higher in
men than in women.
n In another community-based study of 13,929 subjects
also in Japan, the Brugada ECG was found in 98. There
was one death during a follow-up of 2.6 years compared
with 139 deaths among those without the Brugada ECG.
The total mortality of patients with the Brugada ECG
was not different from those without the abnormality.
Wolff-Parkinson-White (WPW) syndrome: The WPW
syndrome is another clinical entity in which malignant ven-
tricular arrhythmias can occur in the absence of structural
cardiac disease that can result in sudden death. The ECG
recognition, mechanism and the different arrhythmias asso-
ciated with the syndrome, is further discussed in Chapter 20,
Wolff-Parkinson-White Syndrome.
Acute Therapy
Ventricular fibrillation: The emergency treatment of pa-
tients with ventricular fibrillation is direct current electrical
defibrillation.
Direct current defibrillation: Direct current unsyn-
chronized shocks set at 360 joules if monophasic (or 200
joules if biphasic) should be delivered immediately. The
ACC/AHA/ESC 2006 guidelines for management of ven-
tricular arrhythmias, recommends that if the initial shock
is unsuccessful, five cycles of cardiopulmonary resuscita-
tion should be provided before delivering the second
shock and if the second shock is also not effective, an-
other five cycles of cardiopulmonary resuscitation is
provided before delivering the third shock. The previous
Ventricular Arrhythmias 305
recommendation was to deliver three shocks in a row
followed by cardiopulmonary resuscitation.
Precordial thump: An initial option, which is a Class IIb
recommendation, is that a single precordial thump can be
delivered by the responder. This can be tried if the patient
cannot be immediately defibrillated. (Class IIb means
that the usefulness or efficacy of the procedure/therapy is
less well established by evidence/opinion.)
Cardiopulmonary resuscitation: If the patient has
been in cardiac arrest for more than 5 minutes, a brief pe-
riod of cardiopulmonary resuscitation is initially recom-
mended before the patient is electrically defibrillated.
Pharmacologic agents:
n Epinephrine: If the arrhythmia is refractory to electri-
cal defibrillation, epinephrine 1 mg is given IV and re-
peated every 3 to 5 minutes while providing continu-
ous cardiopulmonary resuscitation.
n Vasopressin: An alternative is to give vasopressin 40 U
IV given once to substitute for the first or second dose
of epinephrine.
n Amiodarone: If ventricular fibrillation is refractory to
electrical defibrillation, amiodarone is also given IV
with a loading dose of 300 mg or 5 mg/kg and electrical
defibrillation repeated. An additional dose of 150 mg of
amiodarone may be given once only. Amiodarone is
continued at 1.0 mg/minute for 6 hours followed by
0.5 mg/minute for the next 18 hours when the patient
has stabilized. It is not necessary to give amiodarone
routinely if the patient responds to the initial shock
followed by a stable rhythm.
n Electrolytes: After ventricular fibrillation is stabilized,
all electrolyte and acid base abnormalities should be
corrected. Serum potassium should be 4 mEq/L and
magnesium 2.0 mg/dL.
n Beta blockers: Beta blockers, unless contraindicated,
should also be given as prophylactic therapy.
Other measures: There are conditions that may have
precipitated or contributed to the arrhythmia. According
to the ACC/AHA/ESC 2006 practice guidelines on ven-
tricular arrhythmias, the contributing conditions include
6 Hs and 5 Ts. They are Hypovolemia, Hypoxia, Hydrogen
ion (acidosis), Hypo- or hyperkalemia, Hypoglycemia,
Hypothermia, Toxins, Tamponade, Tension pneumotho-
rax, Thrombosis (coronary or pulmonary), and Trauma.
These conditions should be identified and corrected.
Sustained monomorphic VT: The acute treatment of sus-
tained monomorphic VT depends on whether or not the pa-
tient is hemodynamically stable. However, because electrical
cardioversion is so effective in terminating monomorphic VT,
cardioversion should be considered as initial therapy regard-
less of symptoms. Among stable patients with monomorphic
VT, pharmacologic therapy can be an option. If the patient
does not respond to the initial pharmacologic agent, the VT
should be terminated with electrical cardioversion.
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306 Chapter 21
Hemodynamically unstable patients with sustained
monomorphic VT: Unstable patients with monomor-
phic VT who are hypotensive (blood pressure 90 mm
Hg), in pulmonary edema or have symptoms of myocar-
dial ischemia from the tachycardia, the ACC/AHA/ESC
2006 guidelines for ventricular arrhythmias and the
ACC/AHA guidelines for the management of ST eleva-
tion myocardial infarction recommend synchronized car-
dioversion with appropriate sedation starting at 100
joules of monophasic shock followed by escalating energy
levels of 200 to 300 and finally 360 joules, if the initial
shocks are unsuccessful.
Hemodynamically stable: In hemodynamically stable
patients with sustained monomorphic VT, electrical car-
dioversion remains an option. Antiarrhythmic agents,
however, may be considered instead of electrical car-
dioversion. The preferred antiarrhythmic agent will de-
pend on the presence or absence of left ventricular sys-
tolic dysfunction.
n Hemodynamically stable patients with preserved left
ventricular function: The acute pharmacologic treat-
ment of sustained VT for patients who are stable with
good left ventricular systolic function includes pro-
cainamide, amiodarone, lidocaine, or sotalol. Only one
antiarrhythmic agent should be given to minimize the
proarrhythmic effect of multiple drugs. If the chosen
antiarrhythmic agent is not effective, electrical car-
dioversion should be performed to terminate the VT.
n Procainamide: The ACC/AHA/ESC 2006 guidelines
for management of patients with ventricular arrhyth-
mias recommend procainamide as the initial agent in
patients with monomorphic VT who are hemody-
namically stable with good left ventricular function.
This agent receives a Class IIa recommendation.
Procainamide is more effective than amiodarone in
the early termination of stable monomorphic VT.
The maximum loading dose of procainamide should
not exceed 17 mg/kg. The loading dose is given as an
intravenous infusion until the tachycardia is sup-
pressed. The infusion should not exceed 50 mg/
minute or a total loading dose of 1 g over 30 minutes.
This is followed by a maintenance dose of 1 to 4
mg/minute. This drug is preferred among all other
drugs in sustained monomorphic VT if the patient is
stable and has preserved systolic function. It should
not be given when there is systolic left ventricular
dysfunction or there is evidence of heart failure.
n Amiodarone: Amiodarone is one of the few agents
that can be given to patients with good LV function
or with LV dysfunction. Although amiodarone is
the recommended antiarrhythmic agent (Class I)
for stable patients with sustained monomorphic
VT according to the ACC/AHA 2004 practice
guidelines for ST elevation myocardial infarction,
it is not as effective as procainamide for early
termination of stable monomorphic VT according
to the ACC/AHA/ESC 2006 guidelines for ventric-
ular arrhythmias and receives a Class IIa recom-
mendation when the VT is refractory to electrical
cardioversion or if the VT is unstable or recurrent
in spite of therapy with intravenous procainamide
or other drugs. The dose of amiodarone is 150 mg
IV given as a bolus within 10 minutes and may be
repeated every 10 to 15 minutes as needed. This is
followed by an IV infusion of 1 mg/minute for the
next 6 hours and 0.5 mg/minute for the next 18
hours. The total intravenous dose should not ex-
ceed 2.2 g during the first 24 hours.
n Lidocaine: If the monomorphic VT is known to be
due to acute myocardial ischemia or a complica-
tion of acute myocardial infarction, lidocaine may
be given as initial therapy. This agent receives a
Class IIb recommendation according to the
ACC/AHA/ESC 2006 practice guidelines for the
management of patients with ventricular arrhyth-
mias. Lidocaine is given IV at an initial bolus of 1
mg per kg body weight. The initial bolus should
not exceed 100 mg. If the first bolus is unsuccess-
ful, a second bolus of 0.5 to 0.75 mg/kg IV is given
and a third and final bolus may be necessary. The
total IV dose within the first 3 hours should not
exceed 3 mg/kg body weight. The infusion is fol-
lowed by a maintenance dose of 1 to 4 mg/minute.
n Sotalol: This agent is not available in the United
States as an IV preparation. Similar to pro-
cainamide, it should not be given when there is LV
dysfunction. Dosing is discussed in the Appendix:
Commonly Used Injectable Pharmacologic Agents.
n Other options:
n Electrical cardioversion: Even among stable pa-
tients, electrical cardioversion may be considered
as initial therapy instead of giving antiarrhythmic
agents. If antiarrhythmic therapy was decided and
was not effective, the patient should be electrically
cardioverted. In stable patients, low monophasic
energy settings starting at 50 joules can be given
under adequate sedation.
n Temporary pacing: Temporary pacing receives a
Class IIa recommendation for overdrive suppression
in patients refractory to cardioversion or in patients
with recurrent VT in spite of antiarrhythmic therapy.
n Hemodynamically stable patients with impaired left
ventricular function: The acute therapy of patients
with monomorphic VT who are hemodynamically
stable but have systolic LV dysfunction (ejection frac-
tion 40 % or evidence of congestive heart failure) is
limited to amiodarone and lidocaine. Agents that can
further depress systolic function such as sotalol and
procainamide are proarrhythmic and negatively in-
otropic and should not be given.
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n Amiodarone: Dosing is the same as in patients
with normal systolic function.
n Lidocaine: Dosing is the same as in patients with
normal systolic function.
Sustained polymorphic VT: Most patients with polymor-
phic VT are generally unstable because the VT has a rapid rate
and electrical defibrillation is usually necessary unless the VT
is self-terminating. The ACC/AHA guidelines on ST elevation
myocardial infarction recommend 200 joules of monophasic
shock under adequate sedation. This is followed by another
shock of 200 to 300 joules if the initial shock is ineffective and
a third shock of 360 joules if necessary. The more recent
ACC/AHA/ESC 2006 guidelines for the management of ven-
tricular arrhythmias suggest that any unsynchronized shock
should be set to the maximum energy setting, which is 360
joules of monophasic shock, to minimize the risk of ventricu-
lar fibrillation with low level settings. After the tachycardia is
terminated, pharmacologic therapy is also recommended.
The type of pharmacologic agent will depend on whether the
polymorphic VT is associated with normal QTc (regular
polymorphic VT) or prolonged QTc (torsades de pointes).
Regular PVT: Regular PVT (normal QTc) is usually asso-
ciated with myocardial ischemia and should be consid-
ered as the cause of the VT in all patients.
n Reverse myocardial ischemia: Urgent coronary angiog-
raphy, insertion of intraaortic balloon pump, and emer-
gency myocardial revascularization should be considered
as part of the overall treatment of regular polymorphic
VT when there is ischemic heart disease. Anti-ischemic
agents such as beta blockers should be given intra-
venously especially if the polymorphic VT is recurrent.
n Antiarrhythmic agents: Therapy is similar to mono-
morphic VT and includes procainamide, amiodarone,
lidocaine, or sotalol (see treatment of monomorphic
VT). Dosing is similar to monomorphic VT. Intravenous
amiodarone receives a Class I recommendation if the
PVT is recurrent without QT prolongation. Lidocaine
receives a Class IIb recommendation in patients with
acute myocardial infarction or myocardial ischemia.
Torsades de pointes: Although the tachycardia of tor-
sades de pointes and regular polymorphic VT look identi-
cal, treatment of these two arrhythmias are different be-
cause one is associated with prolonged QTc, whereas the
other is not. In patients with torsades de pointes with ac-
quired prolongation of the QT interval, the long QT in-
terval is reversible and the cause should be identified and
eliminated. This is in contrast to congenital long QT syn-
drome where prolongation of the QT may not be re-
versible. Nevertheless, in both congenital and acquired
long QT syndrome, any identifiable cause of QT prolon-
gation should be corrected.
n Reverse myocardial ischemia: Myocardial ischemia
can prolong the QTc and cause polymorphic VT and
should be reversed with the use of anti-ischemic
agents. In congenital prolonged QTc, the tachycardia
Ventricular Arrhythmias 307
is often induced by adrenergic stimulation. Thus, beta
blockers are the agents of choice and should be in-
cluded as baseline therapy in patients with torsades de
pointes unless the drug is contraindicated.
n Correct electrolyte abnormalities: Electrolyte abnor-
malities especially hypokalemia and hypomagnesemia
can prolong the QT interval. If the potassium level is
below 4.0 mEq/L, potassium repletion to 4.5 to 5.0
mEq/L should be considered.
n Antiarrhythmic agents: In torsades de pointes, an-
tiarrhythmic agents that prolong the QT interval such
as Class IA and Class III agents are not only ineffective
but may be fatal. The following are recommended for
torsades de pointes.
n Magnesium: This agent receives a Class IIb recom-
mendation. It may not be effective if the QT is not
prolonged. One to 2 g of magnesium is diluted
with 50 to 100 mL D5W and given IV as a loading
dose. The solution is injected within 1 hour (5 to
60 minutes). The infusion is given more rapidly for
unstable patients. This is followed by 10 to 20 g
within the next 24 hours, even in patients without
hypomagnesemia.
n Lidocaine: This antiarrhythmic agent does not
prolong the QT interval. The dose of lidocaine is
the same as for monomorphic VT.
n Isoproterenol: This usually serves as a bridge before
a temporary pacemaker can be inserted. This is usu-
ally effective as temporary treatment in patients with
acquired long QT syndrome when there is signifi-
cant bradycardia, AV block, or when there are pause-
dependent torsades de pointes. Because isopro-
terenol can cause tachycardia, it should not be given
when the torsades de pointes are not pause depend-
ent or the basic heart rate is not bradycardic. When
the tachycardia is pause dependent, the VT can be
prevented by increasing the heart rate resulting in
overdrive suppression similar to that of an artificial
pacemaker. The drug is given IV at 2 to 10 mcg/
minute. The infusion is titrated according to the de-
sired heart rate that can suppress the tachycardia.
n Phenytoin: Phenytoin is given with a loading dose
of 250 mg diluted in normal saline. The solution is
infused IV over 10 minutes. Additional boluses of
100 mg are given every 5 minutes as necessary
under constant blood pressure and ECG monitor-
ing until a maximum dose of 1,000 mg is given.
Dextrose should not be used as a diluent since
crystallization can occur. The drug should not be
given as a continuous IV infusion.
n Temporary pacemaker: A temporary pacemaker is
inserted transvenously for overdrive pacing. This is
usually effective when torsades de pointes is pause
dependent or the VT occur in the setting of brady-
cardia of 60 bpm.
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308 Chapter 21
TABLE 21.1
Recommended Settings for External Defibrillation According to the ACC/AHA Guidelines for
ST-Elevation Myocardial Infarction
Initial Shock
Ventricular fibrillation or 200 Joules*
pulseless VT (unsynchronized)
Unstable polymorphic VT 200 Joules*
(unsynchronized)
Sustained unstable 100 Joules
monomorphic VT (synchronized)
Sustained stable 50 Joules
monomorphic VT (Synchronized)
*The more recent American College of Cardiology/American Heart Association/European Society of Cardiology 2006 guidelines for management
of ventricular arrhythmias recommend maximal defibrillator settings (360 joules of monophasic shock) if unsynchronized shock is delivered to
minimize the risk of ventricular fibrillation with low settings.
VT, ventricular tachycardia.
The following (Table 21.1) is a summary of the recom-
mended initial and subsequent shocks during electrical car-
dioversion in patients with sustained ventricular arrhyth-
mias according to the 2004 ACC/AHA guidelines on ST
elevation myocardial infarction. All shocks are monophasic.
Long-Term Therapy
Ventricular fibrillation and sustained VT: Patients who
have survived an episode of sustained VT or ventricular fibril-
lation are high risk for sudden death and should be referred to
an electrophysiologist. These patients usually have structural
cardiac disease with severe LV dysfunction. Any reversible
condition that can cause arrhythmia such as electrolyte ab-
normalities, myocardial ischemia, severe blood gas abnor-
malities, or the use of agents that are proarrhythmic should
be identified and corrected. Beta blockers and anticongestive
agents that prolong survival in patients with left ventricular
systolic dysfunction such as angiotensin-converting enzyme
inhibitors, angiotensin receptor blockers, aldosterone antag-
onists, and, among African Americans, a hydralazine/nitrate
combination should be given unless these drugs are con-
traindicated. In patients with poor LV systolic function, im-
plantation of an automatic defibrillator for secondary pre-
vention is recommended. In these patients, the use of
antiarrhythmic agents does not match the efficacy of the au-
tomatic defibrillator in reducing mortality.
Nonsustained VT: Patients who are completely asympto-
matic but have frequent multiformed PVCs with nonsustained
monomorphic VT need to be referred for further cardiac eval-
uation. The arrhythmia is most probably benign in asympto-
matic patients with structurally normal hearts. However, in
patients with impaired LV function, especially those who have
survived an acute myocardial infarction, the patient has to be
referred for further evaluation and therapy. Similarly, in pa-
Second Third
200300 Joules* 360 Joules
(unsynchronized) (unsynchronized)
200300 Joules* 360 Joules
(unsynchronized) (unsynchronized)
Escalating energy levels
(synchronized)
Escalating energy levels
(Synchronized)
tients with PVT, even when nonsustained, treatment and fur-
ther evaluation is warranted. Treatment of systolic dysfunction
with beta blockers, angiotensin-converting enzyme inhibitors,
or angiotensin receptor blockers and aldosterone antagonists
should be considered in addition to correction of myocardial
ischemia or other metabolic, electrolyte, and blood gas abnor-
malities that may be present. No antiarrhythmic therapy is
necessary in asymptomatic patients with nonsustained VT
who have been evaluated to have structurally normal hearts.
PVCs: PVCs from ventricular parasystole is considered a be-
nign finding. Similarly, simple, benign ventricular extrasys-
toles are commonly seen in normal healthy individuals. These
ectopic impulses may be associated with smoking; excessive
coffee, tea, or alcohol; use of diet pills, sympathetic agents,
thyroid hormones, diuretics; and medications for common
colds or asthma, antipsychotic agents and electrolyte abnor-
malities. A previously asymptomatic and presumably healthy
individual with a structurally normal heart who develops pal-
pitations from simple, benign PVCs should be evaluated for
these possible causes. Treatment is simply reassurance that the
arrhythmia is benign and the possible cause eliminated.
Prognosis
Prognosis will depend on the type of ventricular arrhythmia
and the underlying cardiac abnormality.
Sustained VT or ventricular fibrillation are serious and
life-threatening arrhythmias. Most of these arrhythmias
are frequently seen in patients with severe left ventricular
dysfunction and has high mortality. Prognosis is im-
proved with appropriate therapy.
Patients with structurally normal hearts who develop ma-
lignant ventricular arrhythmias are also at risk for sudden
death. These include patients with prolonged QTc,
LWBK271-C21_287-309.qxd 29/1/09 9:23 pm Page 309 LWBK270-4119G-C02_073-110.qxd
Brugada syndrome, and arrhythmogenic right ventricular
cardiomyopathy. Prognosis is improved with medical
therapy. In properly selected patients, implantation of an
automatic defibrillator may be indicated.
In the general population, VT or ventricular fibrillation
can occur as a complication of acute myocardial infarc-
tion and is a common cause of sudden death.
PVCs that are parasystolic are considered benign. Al-
though acute treatment of frequent parasystolic and ex-
trasystolic PVCs and nonsustained VT is not indicated,
long-term prognosis will depend on the presence or ab-
sence of cardiac disease.
PVT with or without QTc prolongation, even when self-
terminating and of short duration, may incur an immedi-
ate risk of morbidity and mortality. The long-term prog-
nosis will depend on the cause of the PVT and underlying
cardiac abnormality.
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Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines
for the management of patients with ST elevation myocardial
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Arizona Center for Education and Research on Therapeutics.
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Bigger JT Jr. Ventricular arrhythmias: classification and general
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Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by
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Conover MB. Monomorphic ventricular rhythms. In: Under-
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18661874.
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281291.
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Zimetbaum PJ, Josephson ME, Kwaku KF. Genetics of congeni-
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22
Wide Complex Tachycardia

Causes of Wide Complex Tachycardia Wide QRS Complex from Ventricular

Tachycardia
Wide complex tachycardia indicates the presence of
fast and regular heart rate of 100 beats per minute
(bpm) associated with wide QRS complexes measuring
at least 120 milliseconds.
A wide complex tachycardia can be ventricular or
supraventricular.
Ventricular tachycardia (VT) has a wide QRS
complex because the arrhythmia originates below
the bifurcation of the bundle of His. The impulse
does not follow the normal atrioventricular (AV)
conduction system and activation of the ventricles
does not occur simultaneously (Fig. 22.1A).
Supraventricular tachycardia (SVT) has narrow
QRS complexes because the impulse originates
above the bifurcation of the bundle of His. The im-
pulse follows the normal AV conduction system and
activation of both ventricles is simultaneous. SVT
can have wide QRS complexes when there is:
n Preexistent bundle branch block (B).
n AV reciprocating tachycardia (AVRT) due to the
presence of a bypass tract. This wide complex
tachycardia is also called antidromic AVRT (C).
n Ventricular aberration or rate related bundle
branch block (D).
Distinguishing VT from wide complex SVT is always a
diagnostic challenge. Unless the patient is unstable, a
12-lead electrocardiogram (ECG) should always be
recorded when there is wide complex tachycardia be-
cause it provides much more diagnostic information
than a single-lead rhythm strip.
Single-lead rhythm strip: Very often, the tachycardia
is recorded only on a rhythm strip obtained from a car-
diac monitor. When only a single-lead ECG is available
for interpretation, any of the following findings is diag-
nostic of VT:
Unusually wide QRS complexes (Fig. 22.2).
Complete AV dissociation (Fig. 22.3).
Ventricular fusion complex (Figs. 22.4 to 22.6).
Sinus captured complex or Dressler beat (Fig. 22.7).
Ventriculoatrial conduction with block (Figs. 22.8
and 22.9).
Unusually wide QRS complexes:
When the tachycardia has a right bundle branch
block (RBBB) configuration, the tachycardia is ven-
tricular if the width of the QRS complex exceeds
0.14 seconds. If the tachycardia has a left bundle

Figure 22.1: Wide Complex Tachy- A B C D

cardia. (A) Ventricular tachycardia.
(BD) Examples of supraventricular (SVT)
with wide QRS complexes. (B) SVT with
preexistent bundle branch block. (C)
Antidromic atrioventricular reciprocating
tachycardia from the presence of a
bypass tract. (D) SVT is conducted with
aberration. ( ) indicates the origin of
the impulse; (arrows) the direction of the
spread of the electrical impulse.
Ventricular Tachycardia Supraventricular Tachycardia

310
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Wide Complex Tachycardia 311

>160 ms

Figure 22.2: Tachycardia with Unusually Wide QRS Complexes. The QRS
complexes are unusually wide measuring >160 milliseconds.This run of tachycardia with un-
usually wide QRS complexes is due to ventricular tachycardia (VT).The first complex (circled)
shows no evidence of preexcitation or preexistent bundle branch block. The star indicates a
fusion complex, which is also diagnostic of VT.

Figure 22.3: Complete Atrioventricular (AV) Dissociation. When complete AV dissoci-

ation is present, the diagnosis of the wide complex tachycardia is ventricular tachycardia. Arrows
point to P waves that are completely dissociated from the QRS complexes.

Figure 22.4: Ventricular Fusion Complex. The QRS complex marked by the star is a ven-
tricular fusion complex. Ventricular fusion complexes are usually seen at the beginning or end of
ventricular tachycardia (VT). When a ventricular fusion complex is present, the wide complex
tachycardia is VT.

Figure 22.5: Ventricular Fusion Complexes. A rhythm strip shows fusion complexes that
are marked by stars. The ventricular fusion complexes can assume any configuration other than
the configuration of the QRS complexes during normal sinus rhythm or during tachycardia. The
presence of a ventricular fusion complex during wide complex tachycardia is diagnostic of ven-
tricular tachycardia.
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312 Chapter 22

Figure 22.6: Ventricular Fusion

Complex. (A) Two separate impulses,
ventricular and supraventricular, simulta-
neously activate the ventricles to cause a
ventricular fusion complex. (B) A fusion
complex occurs when two separate ven-
tricular impulses activate the ventricles
simultaneously. (C) A ventricular fusion
complex is not possible with two
separate supraventricular impulses
because both are obligated to follow the
A B C
same pathway to the ventricles.
Ventricular Fusion Complex Two supraventricular impulses can not
cause a ventricular fusion complex
because they have to follow the same
pathway to the ventricles

Figure 22.7:Sinus Captured A. 12 lead ECG during tachycardia

F F
and Ventricular Fusion
Complexes. (A) 12-lead electrocar-
diogram during wide complex tachy-
F
cardia. Ventricular fusion complexes F F
are marked by the letter F. The fusion
complexes are preceded by sinus P
waves (arrowheads). A sinus captured
F
complex, also called Dresslers beat, is F
circled. (B) Lead II rhythm strip from
the same patient recorded separately
during normal sinus rhythm. The
sinus-captured complex recorded in Lead II during tachycardia Sinus captured
F F complex
lead II is identical to the QRS
complex during sinus rhythm and
are both circled for comparison.
B. Lead II during normal sinus rhythm

Figure 22.8:Wide Complex

Tachycardia with 2:1
Ventriculoatrial (V-A) Block.
V-A conduction is shown in leads
II, III, and aVF.The retrogradely
conducted P waves (arrows)
occur after every other QRS com-
plex representing 2:1 second-
degree V-A block. V-A conduction
with intermittent V-A block is
diagnostic of ventricular
tachycardia.
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2:1 2:1 3:2
Figure 22.9: Ventriculoatrial (V-A) Wenckebach. Lead II rhythm strip shows 2:1 V-A
block and 3:2 V-A Wenckebach (arrows on the left half of the rhythm strip) with gradual prolon-
gation of the R-P interval until a ventricular impulse is not followed by an atrial complex. The
presence of intermittent V-A conduction suggests that the origin of the tachycardia is
ventricular.
branch block (LBBB) configuration, the tachycardia
is ventricular if the QRS complex exceeds 0.16 sec-
onds. There should be no preexistent bundle branch
block or preexcitation in baseline ECG and the pa-
tient should not be taking any antiarrhythmic med-
ication that prolongs intraventricular conduction.
Differentiating a wide complex tachycardia as having
a RBBB or LBBB configuration may be difficult if
only a single-lead monitor strip is available for inter-
pretation (Fig. 22.2). However, an unusually wide
QRS complex measuring >0.16 seconds is usually VT,
regardless of the configuration of the QRS complex.
Ventricular Tachycardia
Complete AV dissociation: When sinus P waves are
present and there is no relationship between the P
waves and the QRS complexes, complete AV dissocia-
tion is present (Fig. 22.3). Complete AV dissociation
occurs when two separate pacemakers are present: one
capturing the atria and the other the ventricles. During
VT, the rate of the ventricles is faster than the rate of
the atria; thus, the slower atrial impulse will usually
find the ventricles refractory. Complete AV dissociation
occurring during a wide complex tachycardia is diag-
nostic of VT.
Ventricular fusion complex: In VT, the sinus impulse
may be able to capture the ventricles if the sinus im-
pulse is perfectly timed to occur when the ventricles are
not refractory. A ventricular fusion complex may occur
if the ventricles are partly activated by the sinus im-
pulse and partly by the VT (Figs. 22.422.6).
Ventricular Fusion Complex
Ventricular fusion complex: A ventricular fusion
complex results when the ventricles are simultaneously
Wide Complex Tachycardia 313
3:2 3:2 3:2
activated by two separate impulses, causing a change in
the pattern of ventricular activation. At least one of the
impulses should originate from the ventricles. A ven-
tricular fusion complex therefore can occur if one im-
pulse is ventricular and the other supraventricular (Fig.
22.6A). It can also occur if both impulses originate
from two different locations in the ventricles (Fig.
22.6B). Two separate supraventricular impulses cannot
produce a ventricular fusion complex because both
supraventricular impulses are obligated to follow the
same conduction pathway on their way to the ventri-
cles and will not alter the pattern of ventricular activa-
tion (Fig. 22.6C). Thus, when a ventricular fusion com-
plex occurs during a wide complex tachycardia, the
diagnosis is VT. The fusion complex can assume any
configuration other than the configuration of the QRS
complex during sinus rhythm or during the wide com-
plex tachycardia. Examples of ventricular fusion com-
plexes are shown in Figures 22.2, 22.4, and 22.5.
Sinus Captured Complex
Sinus captured complex: In VT, the atrium and
ventricles are completely dissociated with the ven-
tricular rate faster than the sinus rate. The sinus im-
pulse is, therefore, unable to capture the ventricles,
because the ventricles are almost always refractory on
arrival of the sinus impulse to the ventricles. If a
properly timed sinus impulse arrives at the ventricles
when the ventricles are not refractory, the sinus im-
pulse may be able to capture the ventricles partially
(resulting in a fusion complex) or completely (result-
ing in sinus captured complex). A sinus-captured
complex during VT is a narrow QRS complex identi-
cal to a normally conducted sinus impulse (Fig.
22.7). Very often, sinus P waves are visible preceding
fusion or sinus captured complexes. The presence of
a sinus-captured complex during wide complex
tachycardia is diagnostic of VT.
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314 Chapter 22

Ventriculoatrial conduction: Ventriculoatrial (V-A)
conduction or conduction of an impulse from ventri-
cles to atria is not commonly seen in the ECG, but has
been shown to occur in 50% of patients with VT dur-
ing electrophysiologic testing. One-to-one V-A con-
duction can occur during VT, but it can also occur dur-
The 12-Lead ECG
ing antidromic or wide complex AVRT. Not generally
known as a marker of VT is V-A conduction with
block.
V-A conduction with block: V-A conduction is better
appreciated when recorded in a 12-lead ECG rather
than a rhythm strip. The retrograde P waves are best
recognized in leads II, III, and aVF. Figure 22.8 shows
2:1 V-A block and Figure 22.9 shows V-A Wenckebach.
V-A block is not possible when there is antidromic
AVRT because the tachycardia will not be able to sus-
tain itself and will terminate if the impulse is blocked
(see Chapter 16, Supraventricular Tachycardia due to
Reentry). The presence of V-A conduction with inter-
mittent block points to the ventricles as the origin of
the arrhythmia and is diagnostic of VT.
The diagrams in Fig. 22.10 summarize the ECG find-
ings of VT when only a rhythm strip is recorded.
Twelve-lead ECG: A full 12-lead ECG provides more
useful information than a single-lead rhythm strip in
differentiating VT from wide complex SVT and
should always be recorded unless the patient is he-
modynamically unstable requiring immediate elec-
trical cardioversion. When a wide complex tachycar-
dia is recorded in a 12-lead ECG, it does not only
provide more information; a more organized ap-
proach to distinguish VT from wide complex SVT
can be used (Fig. 22.11).
If a 12-lead ECG is recorded during a wide complex
tachycardia, the following algorithm proposed by Bru-
gada et al. attempts to diagnose VT in four simple steps
(Fig. 22.11).

> 0.16 sec

Figure 22.10: Wide Complex
Tachycardia. When only a rhythm 1. Unusually
strip is recorded, the following electro- wide QRS
complexes
cardiogram findings are diagnostic of
ventricular tachycardia. (1) Unusually
wide QRS complexes measuring >0.16 P-P Interval
seconds. (2) Complete atrioventricular P
dissociation. (3) Ventricular fusion
2. Complete AV
complex (arrow). (4) Sinus captured
Dissociation
complex (arrow). (5) V-A Wenckebach
(6) Two to one V-A block.The stars
mark the sinus P waves. V-A, Ventricu- Fusion complex
P
loatrial.
3. Ventricular
Fusion
Complex

P Sinus Captured Complex

4. Sinus
Captured
Complex

Retrograde P wave 3:2 V-A Wenckebach

5. V-A
Wenckebach

Retrograde P wave

6. 2:1 V-A Block

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Wide Complex Tachycardia 315

Algorithm for the Diagnosis of VT Figure 22.11: Algorithm for

Wide Complex Tachycardia.
(Modified from Brugada et al.)
I. Look for an RS Complex in V1 to V6

No RS Complex RS Complex is present.

Diagnosis: VT Proceed to Step II

II. Measure Duration of RS Complex

RS Complex >100 ms RS Complex 100 ms

Diagnosis: VT Proceed to Step III

III. Look for AV Dissociation

AV Dissociation No AV Dissociation
Diagnosis: VT Proceed to Step IV

IV. Morphologic Criteria

Right Bundle Branch Block Morphology Left Bundle Branch Block Morphology

Monophasic
V1 V1/V2
R 0.04 RS 0.07 Slurred S
Biphasic

V6

V6
Any Q in V6
qR qr QS R rS

Any pattern in V1 and V6 = VT Any pattern in V1 or V2 and V6 = VT

Step 1: Look for an RS complex in V1 to V6. If there
is no RS complex, the diagnosis is VT and no further
analysis is needed. If an RS complex is present, pro-
ceed to step 2.
Step 2: Measure the RS duration. If the RS duration
is >100 milliseconds, the diagnosis is VT and no fur-
ther analysis is needed. If the RS duration is 100
milliseconds, proceed to step 3.
Step 3: Look for AV dissociation. If there is AV dis-
sociation, the diagnosis is VT and no further analy-
sis is needed. If AV dissociation is not present, pro-
ceed to step 4.
Step 4: The morphologic criteria are used to diag-
nose VT (Figure 22.11)
n If the QRS complex is positive in V1, the mor-
phologic criteria for RBBB are used to diagnose
VT.
n If the QRS complex is negative in V1, the mor-
phologic criteria for LBBB are used to diagnose
VT.
The full algorithm is shown in Figure 22.11. If the diag-
nosis of VT is not possible after going through these
four simple steps, the patient should be further evalu-
ated for other signs of VT using all possible diagnostic
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316 Chapter 22
modalities including history, physical examination,
previous ECG if available, response to vagal maneu-
vers, and certain pharmacologic agents.
If the diagnosis of VT cannot be confirmed, the ECG
should be evaluated for wide complex SVT. If the diag-
nosis remains uncertain after careful evaluation of the
wide complex tachycardia, practice guidelines recom-
mend that the tachycardia should be managed as VT.
Step I: Absence of RS Complex in the
Precordial Leads is VT
The following illustrations will demonstrate step by
step how to diagnose VT using the algorithm.
Step I: Look for an RS complex in the precordial
leads. The first step is to look for RS complex in V1 to V6.
Examples of RS complexes are shown in Figure 22.12.
If RS complex is not present in any precordial lead
V1 to V6, the diagnosis is VT and no further analysis
is necessary (Fig. 22.13).
If RS complex is present in any of the precordial
leads, the diagnosis of VT cannot be confirmed, pro-
ceed to step II.
Step II: RS Duration >100 Milliseconds
is VT
Step II: Measure the RS duration. If an RS complex
is present in any precordial lead, the diagnosis of VT is
not possible. The next step is to measure the duration
of the RS complex. If several RS complexes are present,
the RS complex with the widest duration is selected.
The duration of the RS complex is measured from
the beginning of the R wave to the nadir or lowest
point of the S wave as shown in Figure 22.14.
If the duration of the RS complex is >100 millisec-
onds as shown in Figure 22.15, the diagnosis is VT
and no further analysis is necessary.
If the duration of the RS complex is 100 millisec-
onds, the diagnosis of VT cannot be confirmed, pro-
ceed to step III.
A wide complex tachycardia is shown in Figure 22.16.
The algorithm is applied to look for VT.
Step I: Look for an RS complex. RS complexes are
present in V2 to V5. The diagnosis of VT cannot be
confirmed.
Step II: Measure the duration of the RS complex. V2
is selected because it has the widest RS duration. The
duration of the RS complex is >100 milliseconds. The
diagnosis is VT and no further analysis is needed.
Step III: AV Dissociation is Diagnostic
of VT
Step III: Look for AV dissociation. If VT is not diag-
nosed after steps I and II, the algorithm continues to
step III. Step III of the algorithm is to look for AV
dissociation.
Any of the 12 leads can be used when looking for AV
dissociation. If AV dissociation is present, as shown
in Figure 22.17, the diagnosis is VT and no further
analysis is needed.
If AV dissociation is not present, the diagnosis of VT
cannot be confirmed, proceed to step IV.
Step IV: Morphologic Criteria
Step IV: Morphologic criteria. In the fourth and final
step, the QRS complex is classified as having either
RBBB or LBBB morphology.
The morphology is RBBB if in V1: the QRS complex
is positive or the R wave is taller than the S wave.
The morphology is LBBB if in V1: the QRS complex
is negative or the S wave is deeper than the height of
the R wave.
RBBB morphology: If the tachycardia has a RBBB
morphology, V1 and V6 should be examined for VT.
V1: The following findings in V1 favor VT. Monopha-
sic or biphasic QRS complex. Examples of monopha-
sic and biphasic QRS complexes in V1 are shown in
Figure 22.18.
V6: The following findings in V6 favor VT. Any q
wave (except qrs), monophasic R wave, r/S ratio
1 (r wave smaller than S wave). These changes are
shown in Figure 22.18.
If a monophasic or biphasic QRS pattern is present in
V1  any of the described QRS pattern is present in V6,
the diagnosis is VT. If the pattern is present only in V1,
but not in V6, or the pattern is present only in V6, but
not V1, the diagnosis of VT is not possible.
Step IV: Wide Complex Tachycardia
with RBBB Morphology
The following example (Fig. 22.19) shows how to use
the algorithm when there is a wide complex tachycar-
dia with a RBBB configuration.
Step I, step II, and step III of the algorithm are un-
able to make a diagnosis of VT.
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Wide Complex Tachycardia 317

R
S
Rs
RS
rS

Figure 22.12: RS Complexes. Examples of RS complexes

are shown diagrammatically. Any complex starting with a q wave
or a complex with RSR configuration is not an RS complex.

Use only precordial leads V1 to V6

Figure 22.13: Applying the Al-
gorithm. Step I: Look for an RS
complex in V1 to V6 only. A qR config-
uration is seen in V1, V2, V3, V4, V5, and
V6. Because there is no RS complex in
any of the precordial leads, the diag-
nosis is ventricular tachycardia. No
further analysis is necessary.

Duration of the RS complex
Figure 22.14: RS Complexes. Examples of RS complexes
are shown. The duration of the RS complex is measured from
the beginning of the R wave to the nadir of the S wave.
40 ms > 100 ms
Figure 22.15: Duration of the RS Complex. The duration
of the RS complex is measured from the beginning of the R
wave to the lowest portion of the S wave as shown by the
arrows. One small block in the electrocardiogram is equivalent
to 40 milliseconds and 2.5 small blocks is equivalent to 100 mil-
liseconds. If the RS duration is >100 milliseconds, the diagnosis
is ventricular tachycardia and no further analysis is needed. ms,
milliseconds.
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318 Chapter 22

Figure 22.16: Step II: Measure

the Duration of the RS
Complex. Step I: Look for an RS
complex in the precordial leads. RS
complexes are seen in V2, V3, V4, V5,
and probably V6. Because RS
complexes are present, the diagnosis
of ventricular tachycardia (VT)
cannot be confirmed. Step II: The du-
ration of the RS complex is measured.
V2 has the widest RS duration and is
magnified to show how the RS is
measured. The RS measures 120 mil-
liseconds. The diagnosis is VT and no
further analysis is needed. ms,
milliseconds.

Magnified V2

RS = 120 ms (3 small blocks) 1 small block = 40 ms

A.

B.

Figure 22.17: Step III: Look for Atrioventricular (AV) Dissociation. Step I: Look
for an RS complex. Because an RS complex is present in V1, V2, and V3, the diagnosis of ven-
tricular tachycardia (VT) can not be confirmed. Step II: Measure the duration of the RS
complex. The RS duration in V2 and in V3 is 100 milliseconds. Because the duration of the
RS complex is 100 milliseconds, diagnosis of VT can not be confirmed. Step III: Look for
AV dissociation. (B) This is the same lead II rhythm strip shown in (A) and is magnified to
show the AV dissociation. The P waves (arrows) are completely dissociated from the QRS
complexes. When complete AV dissociation is present, the diagnosis is VT and no further
analysis is necessary. ms, milliseconds.
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Wide Complex Tachycardia 319

Figure 22.18: Morphologic Cri-

V1 V6 teria for Right Bundle Branch
Block Pattern. The morphology
of the QRS complexes that favor
R RR rR Rr qR qr R ventricular tachycardia (VT) is shown
QS
Monophasic R waves
+ R
for V1 and for V6. If a monophasic or
biphasic complex is present in V1
and any of these QRS patterns is also
smaller
Rs qR than S present in V6, the diagnosis is VT.

Biphasic QRS complexes R/S ratio <1

Any pattern in V1+ any pattern in V6 = VT

Figure 22.19: Wide Complex Tachycardia

with Right Bundle Branch Block (RBBB)
Morphology. Step 1: Look for an RS complex.
RS is present in V6. Step 2: Measure the RS dura-
tion. V6 is magnified to show that the RS duration
is 100 milliseconds. Step 3: Look for atrioven-
tricular (AV) dissociation. AV dissociation is not
present. Step 4: Morphologic criteria. Because V1
is positive with a tall R wave, the morphologic
criteria for RBBB are used. In V1, the QRS
morphology is biphasic (QR pattern), which
favors ventricular tachycardia (VT). In V6, the RS
ratio is 1 (r smaller than S). This also favors VT.
V1 and V6 match the morphologic criteria for VT;
therefore, the diagnosis is VT. ms, milliseconds.

Magnified V6

V1 or V2 V6 Figure 22.20: Morphologic Cri-

teria for Left Bundle Branch
Block (LBBB) Configuration.
The diagnosis is ventricular tachycar-
+ qR qr QS qrs
dia if any of the above QRS morphol-
ogy is present in V1 or V2 and any Q
R > 0.04 rS >0.07 Slurred or Any Q wave in V6 wave is present in V6. When the
sec sec notched S wave tachycardia has a LBBB morphology,
it is faster and simpler to check V6
first for any Q wave before matching
Any of the above QRS pattern in V 1 or V2 + any Q wave in V6 = VT the finding in V1 because the only
criterion in V6 is to look for a Q wave.
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320 Chapter 22
Step IV of the algorithm shows RBBB configuration;
thus, the RBBB morphologic criteria are used as
shown in Figure 22.18.
Step IV: Wide Complex Tachycardia
with LBBB Morphology
LBBB Morphology: When the wide complex tachy-
cardia has a LBBB configuration, V1 or V2 can be used.
This is unlike wide complex tachycardia with RBBB
configuration, where only lead V1 is used. The diagno-
sis is VT if any of the following findings is present in V1
or V2 and also in V6 (Fig. 22.20):
V1 or V2:
n R wave duration in V1 or V2 is 0.04 seconds or
40 milliseconds
n RS duration in V1 or V2 is 0.07 seconds or 70
milliseconds
n Slurring or notching of the downslope of the S
wave.
V6: Any q wave in V6 will favor VT (Fig. 22.20). This
may be a qR, qr, QS, or QRS.
If any of these QRS morphologies is present in V1 or V2
 any of the QRS morphologies is present in V6, the di-
agnosis is VT. If the QRS morphology is present only in
Figure 22.21: Applying the Algorithm.
Step IV: Steps I, II, and III of the algorithm are
unable to diagnose ventricular tachycardia (VT).
Step IV: Because the QRS complex in V1 is nega-
tive or the S wave is deeper than the R wave, the
morphologic criteria for left bundle branch block
are used. V6 starts with a q wave. This favors VT.
V1 has RS duration of 0.07 seconds. There is also
notching of the downslope of the S wave in V2
(bold arrow). Either of these findings favors VT.
V12 and V6 match the morphologic criteria for
VT; therefore, the diagnosis is VT.
Magnified V1V2
V1 or V2, but not in V6, or the QRS morphology is pres-
ent only in V6, but not in V1 or V2, the diagnosis of VT
is not possible.
When the tachycardia has LBBB morphology, it is sim-
pler to evaluate V6 before V1 because the only criterion
in V6 is simply to look for any q wave. If a q wave is
not present, the diagnosis of VT is not possible. If the
tachycardia has RBBB morphology, V1 should be in-
spected first because the only criterion in V1 is to look
for a monophasic or biphasic complex.
The ECG in Figure 22.21 shows a wide complex tachy-
cardia with LBBB morphology (rS complex is present
in V1). Steps I to III of the algorithm are unable to make
a diagnosis of VT. Using step IV of the algorithm, the
QRS complex has a LBBB configuration; thus, the mor-
phologic criteria for LBBB are used (see Figure 22.21).
Other Findings Diagnostic of VT
Other findings: If VT cannot be diagnosed after going
through the algorithm, there are other ECG findings
not included in the algorithm that may suggest VT.
RBBB morphology with left axis deviation >30
(Fig. 22.22).
LBBB morphology with right axis deviation >90
(Fig. 22.23).
V6
V1
V2
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Figure 22.22: Right Bundle Branch Block with Left Axis Deviation. This finding favors ventricular tachy-
cardia.
Northwest axis: The QRS axis is between 90 to
180 (Fig. 22.24).
Concordant QRS complexes: All QRS complexes in
V1 to V6 are similar and are all pointing upward
(positive concordance) or downward (negative con-
cordance), as shown in Figures 22.24 and 22.25.
Previous ECG: A previous ECG shows myocardial
infarction (Fig. 22.26) or previous ECG shows that
during sinus rhythm, bifascicular block is present,
which changes in configuration during tachycardia
(Fig. 22.27).
Concordance: Negative concordance implies that all
QRS complexes in the chest leads are pointing down-
Findings Favoring SVT
ward. Positive concordance implies that all the QRS
complexes are pointing upward (Figs. 22.24 and
22.25).
Previous ECG: If myocardial infarction is present in
a previous ECG, the wide complex tachycardia is VT.
This is based on the observation that VT is frequently
associated with structural cardiac disease especially
Wide Complex Tachycardia 321
when there is left ventricular dysfunction (Fig.
22.26).
Previous ECG: If LBBB or a preexistent bifascicular
block such as RBBB plus a fascicular block is present in
a previous ECG and the morphology of the QRS com-
plex changes during the tachycardia, the diagnosis is
VT (Fig. 22.27). This is based on the assumption that
ventricular aberration cannot occur when only one fas-
cicle is intact.
Wide complex SVT: After evaluating the ECG for VT
and the diagnosis of VT cannot be confirmed, the fol-
lowing findings in the 12-lead ECG suggest that the
wide complex tachycardia is supraventricular.
Triphasic pattern in V1 and in V6: SVT with RBBB
configuration has a triphasic rSR pattern in V1 and
Figure 22.23: Left Bundle
Branch Block with Right
Axis >90. This finding usually
indicates ventricular tachycardia
(VT). Note also the presence of
complete AV dissociation
(arrows), which also indicates VT.
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322 Chapter 22

Figure 22.24: Concordance

and Northwest Axis. There is
negative concordance of the QRS
complexes in the precordial
leads (all QRS complexes in V1-V6
are pointing downward with a
left bundle branch block config-
uration). Additionally, the axis of
the QRS complex is between
90 and 180 (northwest axis).
Any of these findings indicates
ventricular tachycardia.

a triphasic qRS pattern in V6 as shown in Figure
22.28. This is diagnostic of SVT.
Rabbits ear: In V1, if the QRS complex has rabbit ear
sign (left ear taller than right ear) or Rr configuration,
the diagnosis is usually VT (Fig. 22.29). If the configu-
ration is rR (right ear taller than left), the finding is
not helpful but could be SVT if V6 is triphasic (qRs) or
R/S ratio is 1 (R wave taller than S wave).
Previous ECG: The diagnosis is SVT if a previous
ECG shows preexistent bundle branch block and the
QRS complexes are identical during tachycardia and
during normal sinus rhythm (Figs. 22.30 and
22.31). The presence of preexcitation in baseline
ECG also suggests that the wide complex tachycar-
dia is supraventricular (Fig. 22.32).
Other Useful Modalities
Preexistent RBBB. If a previous ECG shows preex-
istent RBBB and the QRS pattern during sinus
rhythm is identical to the QRS complexes during
tachycardia, the tachycardia is supraventricular (Fig.
22.30).
Preexistent LBBB: A similar example of wide com-
plex SVT from preexistent LBBB is shown (Fig.
22.31). The configuration of the QRS complexes is
the same during tachycardia and during normal
sinus rhythm.
Preexcitation: When preexcitation is present dur-
ing normal sinus rhythm, the wide complex tachy-
cardia is almost always the result of antidromic
AVRT. Very often, the QRS complex during tachy-
cardia is similar to the QRS complex during normal
sinus rhythm (Fig. 22.32).
In addition to the 12-lead ECG, the following modalities
are helpful in the diagnosis of wide complex tachycardia.
History: The history is often more important than
the ECG in differentiating VT from SVT. The most

Figure 22.25: Concordant

Pattern. There is positive con-
cordance of all QRS complexes
from V1 to V6 (all QRS complexes
are pointing up in V1-V6). Positive
concordance with a right bundle
branch block configuration dur-
ing a wide complex tachycardia is
usually ventricular tachycardia al-
though a wide complex SVT due
to antidromic AVRT is also possi-
ble (see Fig. 22.32).
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Wide Complex Tachycardia 323

A. During tachycardia Figure 22.26: Previous Myocardial In-

farction. (A) A wide complex tachycardia.
(B) A 12-lead electrocardiogram (ECG)
obtained from the same patient during
normal sinus rhythm. QS complexes with ele-
vated ST segments are present in V24. There
are also pathologic Q waves in leads II, III, and
aVF consistent with anterior and inferior my-
ocardial infarctions (MI). When a previous MI is
present by history or by ECG, a wide complex
tachycardia occurring after the MI favors ven-
tricular tachycardia.

B. During normal sinus rhythm

A. Normal sinus rhythm and preexistent LBBB Figure 22.27: Previous Left Bundle
Branch Block (LBBB). (A) Normal sinus
rhythm with LBBB. When a wide complex
tachycardia occurs in a patient with
preexistent LBBB and the configuration of the
QRS complex changes during tachycardia (B),
the diagnosis is ventricular tachycardia. This is
based on the assumption that when there is
bifascicular block, the impulse is obligated to
follow the only remaining fascicle, thus
ventricular aberration as a cause of the tachy-
cardia is not possible.
B. During tachycardia
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324 Chapter 22

R R
R
r A
q
V1
S
+ V6
S
rSR qRS
Figure 22.28: Wide Complex Supraventricular Tachy-
cardia (SVT). Triphasic rSR pattern in V1 combined with
triphasic qRS pattern in V6 favor the diagnosis of SVT.
important feature in the history that will favor VT is
the presence of a previous MI.
n If the patient had a previous MI and the tachy-
cardia occurred after the MI, the diagnosis is VT.
n If the patient has history of tachycardia and has
preexcitation, the diagnosis is SVT.
Physical examination: The presence of hemody-
namic instability does not differentiate ventricular
from supraventricular tachycardia with a wide QRS
complex. The following physical findings however
are diagnostic of VT.
n Cannon A waves
n Varying intensity of the first heart sound
n Varying volume of the arterial pulse
r R
r
B
V1 V1
Rr rabbit ear sign favors VT rR is not helpful but is SVT
if V6 is triphasic or R>S
Figure 22.29: Wide Complex Supraventricular Tachycar-
dia (SVT). (A) When lead V1 shows Rr (left rabbits ear taller than
right rabbits ear), the pattern favors ventricular tachycardia. (B) If
lead V1 shows rR (also called right rabbit ear taller than left rabbit
ear), the finding is not specific but could be SVT if V6 is triphasic
(qRS) or the R wave is taller than S wave (R/S ratio 1).
Vagal stimulation: If the wide complex tachycar-
dia is due to SVT, vagal stimulation may terminate
the arrhythmia or may cause significant slowing of
the heart rate. This will allow the arrhythmia to be
diagnosed more appropriately (Fig. 22.33). The
rhythm should be recorded during vagal stimula-
tion.
Pharmacologic agents: Adenosine, a short-acting
AV nodal blocker, is useful in terminating wide
complex SVT that are AV nodaldependent. The

Figure 22.30: Wide Complex A. During normal sinus rhythm

Supraventricular Tachycardia (SVT) from
Preexistent Right Bundle Branch Block
(RBBB). Electrocardiogram (A) and (B) are from
the same patient. Note that the configuration of
the QRS complexes during normal sinus rhythm
(A) is identical to the QRS complexes during
tachycardia (B) because of preexistent RBBB.

B. During tachycardia
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Wide Complex Tachycardia 325

A. During normal sinus rhythm Figure 22.31: Wide Complex

Supraventricular Tachycardia (SVT) from
Preexistent Left Bundle Branch Block
(LBBB). Electrocardiogram (A) and (B) are from
the same patient. Figure (A) shows the patient
during normal sinus rhythm and (B) during
tachycardia. Note that the configuration of the
QRS complexes during the tachycardia (B) is the
same as during normal sinus rhythm (A) consis-
tent with SVT with preexistent LBBB.

B. During tachycardia

A. During normal sinus rhythm

Figure 22.32: Wide Complex Supraventric-
ular Tachycardia (SVT) from a Bypass
Tract. (A) Normal sinus rhythm with short PR in-
terval and delta waves (arrows) from
preexcitation. (B) From the same patient during
wide complex tachycardia. The presence of preex-
citation in baseline electrocardiogram suggests
that the wide complex tachycardia is due to
antidromic atrioventricular reciprocating
tachycardia.

B. During tachycardia
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326 Chapter 22

Figure 22.33: Wide Complex Tachycardia from Atrial Flutter. Carotid sinus
stimulation can slow the ventricular rate transiently resulting in lengthening of the R-R intervals.
This will allow the baseline to be inspected for atrial activity. Atrial flutter waves can be demon-
strated during transient lengthening of the R-R interval (arrows). The tachycardia is due to atrial
flutter and the wide QRS complexes are due to preexistent bundle branch block.

tachycardia should be recorded while adenosine is
being injected. The cause of the tachycardia may be
identified even if the tachycardia does not respond
to adenosine (Fig. 22.34).
If the diagnosis of the wide complex tachycardia re-
mains uncertain after careful evaluation of all available
clinical information, practice guidelines recommend
that the patient should be treated as VT.
Pharmacologic Agents
Figure 22.34 shows a wide complex tachycardia from
SVT diagnosed with injection of adenosine, a short-
acting AV nodal blocker. It should be given only if
the wide complex SVT is known to be supraventric-
ular in origin. It should not be given if the diagnosis
is uncertain. It is also helpful in identifying the
mechanisms of other types of wide complex tachy-
cardia by slowing the heart rate, as shown in Figure
22.34B.
Wide Complex Tachycardia
Summary of ECG Findings
VT: Any of the following ECG findings suggests VT:
Complete AV dissociation
Ventricular fusion complex
Sinus captured complex
Ventriculoatrial conduction with second degree block
Wide QRS complexes measuring >140 milliseconds when
the tachycardia has a RBBB pattern or >160 milliseconds

Figure 22.34: Wide Complex Tachycardia A. Wide complex tachycardia

and Intravenous Adenosine. (A) Twelve-
lead electrocardiogram showing a wide complex
tachycardia. (B) Leads I, II, and III were recorded
while adenosine was being injected
intravenously. Although the ventricular rate
slowed significantly, the configuration of the QRS
complexes remained unchanged because of pre-
existent bundle branch block. Arrows point to the
presence of atrial tachycardia with a rate of 167
beats per minute. The atrial rate is the same as the
rate of the wide complex tachycardia.

B. Adenosine IV
I

II

III
LWBK271-C22_310-330.qxd 29/1/09 7:48 pm Page 327 LWBK270-4119G-C02_073-110.qxd
when the tachycardia has a LBBB pattern. This observa-
tion is not helpful if there is preexistent bundle branch
block, preexcitation, or the patient is taking antiarrhyth-
mic medications that prolong intraventricular conduc-
tion such as type IA or IC agents.
If there is no RS complex in the precordial leads.
If RS complex is present in the precordial leads and the RS
duration measures >100 milliseconds.
If the QRS complex in V1 has RBBB configuration that is
monophasic or biphasic and the configuration in V6 is qR,
QS, monophasic R wave or rS (R/S 1).
When there is LBBB morphology with right axis devia-
tion >90 or >60.
When there is RBBB morphology with left axis deviation
>30.
If the axis of the QRS complex is between 90 and 180
also called northwest axis.
When QRS complexes are concordant in the precordial
leads:
n LBBB morphology: When the QRS complexes in the
precordial leads are negatively concordant with LBBB
morphology, this is almost always from VT.
n RBBB morphology: When the QRS complexes are
positively concordant with RBBB morphology, this is
usually VT although wide complex SVT from an-
tidromic AVRT is also possible.
If a previous 12-lead ECG is available, the diagnosis is VT if:
n A previous myocardial infarction (MI) is present.
n Bifascicular block is present during normal sinus rhythm
(LBBB or RBBB  a fascicular block) and the QRS mor-
phology becomes different during the tachycardia.
SVT: Any of the following ECG findings is consistent with
SVT:
The tachycardia has RBBB configuration with a triphasic
rSR pattern in V1 and a triphasic qRS pattern in V6.
In V1, right rabbit ear is taller than left. In V6, there is a
triphasic QRS complex or R wave is taller than S wave
(R/S ratio >1).
When a previous 12-lead ECG is available, the diagnosis is
SVT if:
n Bundle branch block is present during normal sinus
rhythm and the QRS configuration is identical during
tachycardia (wide complex SVT from preexistent bun-
dle branch block).
n Preexcitation or Wolff-Parkinson-White (WPW) ECG
is present during normal sinus rhythm (antidromic
AVRT).
Mechanism
Complete AV dissociation: In VT, the ventricles are driven
by an impulse that is faster and separate from that of the
atria. Generally, the atria continue to be controlled by nor-
mal sinus rhythm, which has a slower rate and is independ-
Wide Complex Tachycardia 327
ent from the ectopic activity occurring in the ventricles. The
presence of two independent pacemakers, one controlling
the atria and the other the ventricles, will result in complete
AV dissociation.
Wide QRS complexes: Ventricular tachycardia has wide
QRS complex because the ventricles are driven by an impulse
occurring below the bifurcation of the bundle of His. Thus,
the ventricles are not activated simultaneously because the
impulse has to spread from one ventricle to the other ventri-
cle outside the normal conduction system. This causes the
QRS complexes to be wide measuring 120 milliseconds.
Absence of RS complex in the precordial leads: Absence
of RS complex in the precordial leads indicates VT. When this
occurs, the QRS complex usually starts with a q wave. The q
waves indicate that the ectopic ventricular impulse originates
from the epicardium and spreads from epicardium to endo-
cardium, causing q waves in the precordial leads. This is in
contrast to SVT, which usually activates the ventricles
through the His-Purkinje system and therefore the spread of
the ventricular impulse is from endocardium to epicardium,
causing an RS complex to be inscribed in at least one of the
precordial leads.
Wide RS interval: The RS interval, measured from the be-
ginning of the R wave to the lowest point of the S wave is
equivalent to the spread of the impulse across the thickness
of the myocardium. If the RS interval exceeds 100 millisec-
onds, the diagnosis is VT. This is based on the assumption
that in VT, activation of the ventricles will be less efficient
and will take longer because the impulse is propagated by
muscle cell to muscle cell conduction, as opposed to SVT
where activation of the myocardium will be faster because
the impulse is conducted through the more efficient His-
Purkinje system.
Fusion and sinus captured complexes: Although the
atrial rate or the rate of the sinus impulse is slower than the
rate of the ventricles during VT, a properly timed sinus im-
pulse may arrive at the ventricles when the ventricles are not
refractory and may be able to capture the ventricles partially
(resulting in fusion complexes) or completely (resulting in
sinus captured beats). Thus, when fusion or sinus captured
complexes are present, the diagnosis is VT.
V-A conduction: When there is VT, the ventricular impulse
may be conducted to the atria retrogradely across the AV
node, causing the atria to be activated from below upward.
This will result in inverted P waves in leads II, III, and aVF.
V-A conduction is not uncommon during VT. Wellens et al.
showed that in 70 patients with VT, approximately 50% had
V-A conduction during electrophysiologic testing, with 23
having 1:1 V-A conduction, 7 having 2:1 V-A, conduction,
and 2 having V-A Wenckebach. V-A block may occur sponta-
neously. It could also be induced by carotid sinus pressure.
One to one V-A conduction is not diagnostic of VT because
this can also occur in wide complex AVRT. However, inter-
mittent V-A conduction from V-A block is diagnostic of VT.
V-A block is not generally known as a marker of VT because
V-A conduction is not commonly seen in the surface ECG.
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328 Chapter 22
Clinical Findings
Other modalities that are useful in differentiating VT
from wide complex SVT: Although the 12-lead ECG serves
as the foundation for differentiating VT from wide complex
SVT, there are other modalities that are also useful. These in-
clude the history, physical examination, response to carotid
sinus pressure, and other vagal maneuvers.
Clinical presentation: The hemodynamic condition of
the patient is not reliable in distinguishing VT from SVT.
A patient presenting with hypotension, dizziness, or syn-
cope does not necessarily imply that the tachycardia is
ventricular. Conversely, a patient who is hemodynami-
cally stable during the tachycardia does not necessarily in-
dicate that the tachycardia is supraventricular. When the
heart rate is very rapid (usually 150 beats per minute),
patients usually become symptomatic and even patients
with SVT may become hemodynamically unstable when
there is associated left ventricular systolic or diastolic dys-
function.
Acute Therapy
History: The history is often more important than the
ECG in differentiating VT from wide complex SVT.
n History of previous MI favors VT. The tachycardia
should occur after (not before) the onset of the MI.
n History of preexcitation (WPW syndrome) indicates
wide complex SVT.
Physical examination: The following physical findings
suggest VT. The findings are based on the presence of AV
dissociation, which is very specific for VT.
n Cannon A waves in the neck veins: When atrial and
ventricular contractions are completely dissociated,
simultaneous contraction of the atria and ventricles
may occur intermittently. When atrial contraction is
simultaneous with ventricular contraction, cannon
A waves will appear in the neck representing con-
traction of the atria against a closed tricuspid valve.
This is manifested as intermittent prominent pulsa-
tions in the neck veins.
n Varying intensity of the first heart sound. Another
sign of AV dissociation is varying intensity of the first
heart sound. The mechanism for the varying intensity
of the first heart sound has been previously discussed
in Chapter 8, Atrioventricular Block. The first heart
sound is due to closure of the AV valves and the inten-
sity depends on the position of the valves at the onset
of systole. If the AV valves are widely open when sys-
tole occurs, the first heart sound will be loud. If the AV
valves are almost closed at the onset of systole, the first
heart sound will be very soft. Because the atrial kick (P
wave) pushes the AV valves away from their coapta-
tion points, a short PR interval will cause the ventri-
cles to contract immediately when the AV valves are
widely open, which will result in a loud first heart
sound. If the PR interval is unusually prolonged, the
AV valves will float back to a semiclosed position be-
fore the onset of ventricular contraction; thus, the first
heart sound will be softer. Because AV dissociation is
associated with varying PR intervals, the position of
the AV valves at the onset of systole will be variable;
hence, the intensity of the first heart sound will also be
variable.
n Varying pulse volume: If atrial contraction is per-
fectly timed to occur just before ventricular contrac-
tion, ventricular filling is augmented and a larger vol-
ume is ejected. Because the PR interval is variable
when there is AV dissociation, atrial contribution to
left ventricular filling will vary resulting in varying
pulse volume.
Carotid sinus pressure and other vagal maneuvers:
Another method of distinguishing VT from SVT is to per-
form vagal maneuvers including carotid sinus pressure.
These procedures may terminate wide complex SVT, but
not VT.
Immediate therapy depends on the clinical presentation of
the patient.
Unstable patient: If the patient is unstable with hy-
potension or gross heart failure or the patient is having
symptoms of severe ischemia related to the tachycardia,
electrical cardioversion is indicated whether the wide
complex tachycardia is ventricular or supraventricular.
Stable patient: If the patient is stable, pharmacologic
therapy can be used. Elective cardioversion is also an op-
tion in stable patients if the tachycardia is due to VT or
there is uncertainty about the etiology of the wide com-
plex tachycardia. Carotid sinus stimulation and other va-
gal maneuvers are also helpful and should be tried ini-
tially to terminate SVT. It is also helpful in distinguishing
VT from wide complex SVT.
Pharmacologic therapy: Among stable patients, the type
of pharmacologic agent will depend on whether the tachy-
cardia is known to be ventricular, supraventricular, or the
etiology of the wide complex tachycardia remains uncertain.
Wide complex tachycardia due to SVT: The treatment
for wide complex SVT is similar to the treatment of nar-
row complex SVT. Carotid sinus pressure may terminate
the arrhythmia and should be attempted before intra-
venous medications are given. If the arrhythmia cannot
be terminated with vagal maneuvers, the drug of choice is
adenosine given intravenously. If adenosine is not effec-
tive, another AV nodal blocker may be given. The choice
of the AV nodal blocking agent will depend on the pres-
ence or absence of LV dysfunction as described under the
treatment of narrow complex SVT.
n Wide complex tachycardia due to antidromic AVRT:
If the wide complex SVT is due to antidromic AVRT
(WPW syndrome), the AV node may not be part of
the reentrant circuit (see the Wide Complex or
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Wide Complex Tachycardia 329

Antidromic AVRT section in Chapter 20, Wolff-
Parkinson-White Syndrome). In antidromic AVRT,
anterograde conduction of the atrial impulse occurs at
the bypass tract and retrograde conduction from ven-
tricle to atrium may occur through another bypass
tract instead of the AV node especially when there is
Ebsteins anomaly. Thus, the use of AV nodal blockers
will not be effective because the AV node is not part of
the reentrant circuit. Type IA, type IC, and type III an-
tiarrhythmic agents that will block conduction
through the bypass tract are effective agents in termi-
nating the tachycardia. Procainamide, ibutilide, and
flecainide are the preferred agents.
n The intravenous administration of calcium channel
blockers, beta blockers, or adenosine may not be ap-
propriate unless the tachycardia is definitely SVT be-
cause these pharmacologic agents are not only ineffec-
tive, but may also cause hemodynamic instability or
even death if the wide complex tachycardia turns out
to be VT.
Wide complex tachycardia from VT: If the wide com-
plex tachycardia has been shown to be ventricular in ori-
gin, the acute treatment is similar to monomorphic VT.
The choice of antiarrhythmic agent will depend on the
presence or absence of heart failure or left ventricular dys-
function as discussed in Chapter 21, Ventricular Arrhyth-
Prognosis
mias. For stable patients, procainamide and sotalol are
preferred agents, although amiodarone is also acceptable
and becomes the preferred agent when there is left ven-
tricular dysfunction or heart failure.
Diagnosis uncertain: If the diagnosis of the wide com-
plex tachycardia remains uncertain, calcium channel
blockers, beta blockers, or other agents for terminating
SVT should not be tried because these agents can cause
hemodynamic instability, especially when there is left
ventricular dysfunction. In patients who are hemody-
namically unstable, electrical cardioversion with appro-
priate sedation is recommended (Class I). In stable pa-
tients, the preferred agents are either procainamide or
amiodarone because both agents are effective for VT or
SVT. Intravenous procainamide is recommended as ini-
tial therapy in stable patients. Intravenous amiodarone is
recommended in patients who are hemodynamically un-
stable, refractory to electrical cardioversion, or if the ar-
rhythmia is recurrent in spite of IV procainamide. Lido-
caine is reserved for wide complex tachycardia in patients
with poor left ventricular function associated with acute
MI or myocardial ischemia. Electrical cardioversion is
also an option even if the patient is hemodynamically sta-
ble or if the patient does not respond to the chosen an-
tiarrhythmic medication (Table 22.1).
Electrolyte abnormalities, myocardial ischemia, blood gas,
and other metabolic disorders should be identified and cor-
rected. Medications that may be proarrhythmic should be
eliminated.
Prognosis for VT is worse than SVT. Sustained VT is usually
associated with structural cardiac disease such as acute my-
ocardial infarction, cardiomyopathy, or other myocardial
diseases resulting in impaired systolic function. The presence
of ventricular tachycardia in this setting is associated with a
high mortality. These patients are candidates for implantation

TABLE 22.1

Acute Management of Wide Complex Tachycardia of Uncertain

Diagnosis According to the ACC/AHA/ESC Practice Guidelines in the
Management of Patients with Supraventricular Arrhythmias
Clinical Recommendation Level of Recommendation
Unstable patients DC electrical cardioversion Class I
Stable patients Procainamide Class I
Sotalol Class I
Amiodarone Class I
DC cardioversion Class I
Lidocaine Class IIb
Adenosine Class IIb
Beta blockers Class III
Verapamil Class III
Patients with Amiodarone Class I
poor LV function DC cardioversion Class I
Lidocaine
All pharmacologic agents are given intravenously.
ACC, American College of Cardiology; AHA, American Heart Association; ESC, European Society of
Cardiology; LV, left ventricular; DC, direct current.
LWBK271-C22_310-330.qxd 29/1/09 7:48 pm Page 330 LWBK270-4119G-C02_073-110.qxd
330 Chapter 22
of automatic implantable defibrillator. Overall prognosis de-
pends on the underlying cardiac disease and severity of left
ventricular dysfunction.
If the wide complex tachycardia is due to SVT, prognosis is
the same as for narrow complex SVT.
Suggested Readings
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Baltazar RF, Javillo JS. Images in cardiology. Ventriculo-atrial
Wenckebach during wide complex tachycardia. Clin Cardiol.
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Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
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the Management of Patients with Supraventricular Arrhyth-
mias) J Am Coll Cardiol. 2003;42:14931531.
Brugada P, Brugada J, Mont L, et al. A new approach to the dif-
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Edhouse J, Morris F. ABC of clinical electrocardiography. Broad
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Garratt CJ, Griffith MJ, Young G, et al. Value of physical signs in
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Gozensky C, Thorne D. Rabbit ears: an aid in distinguishing
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Griffith MJ, Garratt CJ, Mounsey P, et al. Ventricular tachycardia
as default diagnosis in broad complex tachycardia. Lancet.
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Guidelines 2000 for cardiopulmonary resuscitation and emer-
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I-158I-165.
Harvey WP, Ronan JA, Jr. Bedside diagnosis of arrhythmias.
Prog Cardiovasc Dis. 1966;8:419445.
Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia:
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41:130144.
Tchou P, Young P, Mahmud R, et al. Useful clinical criteria for
the diagnosis of ventricular tachycardia. Am J Med. 1988;84:
5356.
Wellens HJ. Electrocardiographic diagnosis of arrhythmias. In:
Topol EJ, ed. Textbook of Cardiovascular Disease. 2nd ed.
Philadelphia: Lippincott William & Wilkins; 2002:1665
1683.
Wellens HJJ, Bar FWHM, Lie KI. The value of the electrocardio-
gram in the differential diagnosis of a tachycardia with a
widened QRS complex. Am J Med. 1978;64:2733.
Wellens HJJ, Conover MB. Wide QRS tachycardia. In: The ECG
in Emergency Decision Making. Philadelphia: WB Saunders
Co; 1992:3772.
WHO/ISC Task Force. Definition of terms related to cardiac
rhythm. Am Heart J. 1978;95:796806.
Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006
guidelines for management of patients with ventricular ar-
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port of the American College of Cardiology/American Heart
Association Task Force and the European Society of Cardiol-
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LWBK271-C23_331-378.qxd 29/1/09 7:17 pm Page 331 LWBK270-4119G-C02_073-110.qxd
Acute Coronary Syndrome: ST
Elevation Myocardial Infarction
The Electrocardiogram (ECG) in Acute
Coronary Syndrome
When a patient presents to the emergency department
with chest discomfort or symptoms suspicious of acute
myocardial infarction (MI), the standard of care requires
that a full 12-lead ECG be obtained and interpreted
within 10 minutes after the patient enters the medical fa-
cility. The ECG can provide the following useful informa-
tion in patients with acute coronary syndrome:
The ECG is the only modality capable of making a
diagnosis of ST elevation MI. It is the most impor-
tant tool in defining the onset of the coronary event
and the urgency for immediate revascularization. It
serves as the only basis for deciding whether or not
the patient is a candidate for thrombolytic therapy
or primary angioplasty. It therefore remains central
to the decision making process in managing patients
with acute coronary syndrome.
It provides useful information on whether or not
reperfusion therapy has been successful.
It can identify the culprit vessel, localize whether the
lesion is proximal or distal, and therefore predicts
the extent of jeopardized myocardium. Localizing
the culprit vessel will also help in predicting poten-
tial complications that may inherently occur based
on the geographic location of the MI.
Non-ST Elevation Vessel Lumen is Partially Occluded
Vulnerable Plaque
Plaque Rupture
ST Elevation Vessel Lumen is Completely Occluded
23
It is the simplest and most useful tool in the diagno-
sis of right ventricular MI.
It is the most useful modality in identifying several
complications of acute MI, including the various
atrioventricular and intraventricular conduction ab-
normalities as well as the different bradycardias and
tachycardias, which are frequent during hospitaliza-
tion especially after the initial onset of symptoms.
In this era of modern and expensive technology, the ECG
remains the most important and least expensive modal-
ity in evaluating and managing patients suspected of hav-
ing acute symptoms from coronary artery disease. The
ECG therefore remains the cornerstone in evaluating and
managing patients with acute coronary syndrome and
continues to provide very useful information that is not
obtainable with other more expensive technologies.
Acute Coronary Syndrome
It is well recognized that acute coronary syndrome is
caused by rupture of an atheromatous plaque, resulting
in partial or total occlusion of the vessel lumen by a
thrombus. Depending on how severely the coronary
flow is compromised, varying degrees of myocardial is-
chemia will occur resulting in ST elevation MI, non-ST
elevation MI, or unstable angina (Fig. 23.1).
Figure 23.1:Electrocardiogram
Changes of Acute Coronary
Syndrome. Complete occlusion of
the vessel lumen by a thrombus
causes ST elevation whereas partial
occlusion of the vessel lumen will re-
sult in ST depression, T-wave
inversion, or other less-specific ST
and T-wave abnormalities.
ECG
331
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332 Chapter 23
Figure 23.2: Myocardial Ischemia with ST Ele-
vation. ST elevation from an occlusive thrombus is
persistent and generally does not resolve with coro-
nary vasodilators, whereas ST elevation from coronary
vasospasm is usually transient and responds to coro-
nary vasodilators.
Persistent ST Elevation
Thrombotic Occlusion
of the Vessel Lumen
Emergent Reperfusion
ST elevation MI: Acute ischemia associated with el-
evation of the ST segment indicates complete occlu-
sion of the vessel lumen by a thrombus with com-
plete cessation of coronary blood flow. When this
occurs, myocardial necrosis with elevation of car-
diac markers is always expected.
Non-ST elevation: When acute ischemia is asso-
ciated with ST depression, T wave inversion or
other less specific ST and T wave abnormalities,
partial or incomplete occlusion of the vessel lu-
men by a thrombus has occurred. This type of is-
chemia may or may not be accompanied by cellu-
lar necrosis. When there is cellular necrosis, with
increased cardiac markers in the circulation, non-
ST elevation MI is present. When there is no evi-
dence of myocardial necrosis, the clinical picture
is unstable angina. The diagnosis of myocardial
necrosis is based on the presence of increased car-
diac troponins in the circulation. Regardless of
symptoms or ECG findings, the diagnosis of acute
MI is not possible unless these cardiac markers
are elevated.
ST Segment Elevation
Acute coronary syndrome with elevation of the ST seg-
ment is almost always from complete occlusion of the
vessel lumen by a thrombus resulting in complete cessa-
tion of coronary flow. It can also occur when there is
coronary vasospasm (Fig. 23.2).
ST elevation from occlusive thrombus: ST eleva-
tion from an occlusive thrombus almost always re-
sults in cellular necrosis. Cardiac markers are ex-
pected to be always elevated. Unless the occluded
vessel is immediately reperfused, pathologic Q
waves will occur. ST elevation MI therefore is syn-
onymous with a Q-wave MI.
ST Elevation due to Acute
Myocardial Ischemia
Nitroglycerin
ST Elevation Normalizes
Coronary Vasospasm
Reperfusion not Indicated
ST elevation from coronary vasospasm: ST el-
evation from coronary vasospasm, also called
Prinzmetal angina, is usually transient and can be
reversed with coronary vasodilators such as nitro-
glycerin. Myocardial necrosis usually does not occur
unless vasospasm becomes prolonged lasting more
than 20 minutes.
The presence of ST segment elevation accompanied by
symptoms of myocardial ischemia indicates that the
whole thickness of the myocardium is ischemic. This
type of ischemia is also called transmural ischemia.
Example of ST elevation due to coronary vasospasm is
shown below (Figs. 23.3 and 23.4). The pattern of ST el-
evation is identical and cannot be differentiated from
the ST elevation associated with an occlusive thrombus.
ECG Changes in ST Elevation MI
ST elevation from an occlusive thrombus: When a
coronary artery is totally occluded by a thrombus,
complete cessation of blood flow occurs. Unless ade-
quate collaterals are present, all jeopardized myocar-
dial cells supplied by the coronary artery will undergo
Minutes
Figure 23.3: Coronary Vasospasm. ST elevation from
coronary vasospasm is indistinguishable from ST elevation from
an occlusive thrombus. ST elevation from coronary vasospasm,
however, is usually transient and can be reversed by
nitroglycerin, whereas ST elevation from an occlusive thrombus
is usually persistent and unresponsive to coronary vasodilators.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 333

A. Coronary
Figure 23.4:
Vasospasm. Electrocardiogram
A and B are from the same patient.
(A) ST elevation in multiple leads
(arrows), which may be due to an oc-
clusive thrombus or coronary
vasospasm. (B) After nitroglycerin
was given.The ST segment elevation
has completely resolved within min-
utes consistent with coronary
vasospasm. Coronary angiography
showed smooth walled coronary ar-
B.
teries with no occlusive disease.

irreversible necrosis, usually within 6 hours after the
artery is occluded.
Necrotic changes in the myocardium are usually not
microscopically evident during the first 6 hours after
symptom onset. The cardiac troponins may not even
be elevated in the circulation in some patients. The
ECG, however, will usually show the most dramatic
changes at this time. The ECG therefore is the most im-
portant modality in triaging patients with chest pain
symptoms and is crucial to the diagnosis of ST eleva-
tion MI. It also serves as the main criteria in deciding
whether or not thrombolytic agent or primary coro-
nary angioplasty is needed.
When a coronary artery is completely occluded, the fol-
lowing sequence of ECG changes usually occurs unless
the occluded artery is immediately reperfused (Fig. 23.5):
Peaked or hyperacute T waves (Fig. 23.5A)
Elevation of the ST segments (Fig. 23.5B,C)
Changes in the QRS complex with development of
pathologic Q waves or decrease in the size or ampli-
tude of the R waves (Fig. 23.5D)

Development of pathologic Q
Hyperacute Hyperacute T waves waves, decreased amplitude of
T Wave with ST Elevation the R waves and further ST and
T wave changes

Minutes Minutes Hours Hours

to to to to
Hours Hours Days Days

A B C D E

Figure 23.5: ST Elevation Myocardial Infarction (MI). Giant or hyperacute T waves mark
the area of ischemia (AC) followed by ST elevation (B, C), diminution of the size of the R wave
(D) or development of pathologic Q waves (E) and inversion of the T waves (D, E). The evolution
of ST elevation MI from hyperacute T waves to the development of pathologic Q waves may be
completed within 6 hours after symptom onset or may evolve more slowly for several days.
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334 Chapter 23

Figure 23.6: (A) Hyperacute T A

Waves. The initial electrocardiogram
(ECG) of a patient presenting with
acute onset of chest pain is shown.
Tall, hyperacute T waves (arrows) are
seen in V1 to V4 with elevation of the
ST segments in V34. Note that the hy-
peracute T waves are confined to the
distribution of the occluded vessel
and are usually the first to occur be-
fore the ST segments become
elevated. Subsequent ECGs are
shown in (BD). (B) ST elevation
Myocardial Infarction (MI). This
B
tracing was recorded 15 minutes af-
ter the initial ECG. In addition to the
hyperacute T waves, ST elevation has
developed in V1 to V4 (arrows).
(continued)

Further changes in the ST segment and T waves
(Fig. 23.5D,E)
Peaked or hyperacute T waves: One of the earliest
ECG abnormalities to occur in ST elevation MI is
the development of tall and peaked T waves overlying
the area of ischemia (Fig. 23.6A). These hyperacute T
waves usually precede or accompany the onset of ST
segment elevation and are useful in identifying the
culprit vessel and timing the onset of acute ischemia.
ST segment elevation: Hyperacute T waves are
accompanied or immediately followed by ST seg-
ment elevation. ST segment elevation with symptoms
of chest discomfort indicates an acute process. The
leads with ST elevation are usually adjacent to each
other and mark the area of injury and are helpful in
identifying the culprit vessel. The extent of ST seg-
ment elevation is also helpful in predicting the severity
of myocardial involvement.
Thrombolytic Therapy
ST elevation from acute coronary syndrome is a
medical emergency requiring immediate reperfusion
of the occluded artery with a thrombolytic agent or
with primary percutaneous coronary intervention
(PCI). The extent of myocardial necrosis can be mini-
mized if reperfusion of the occluded artery is timely
and successful.
Thrombolytic Therapy: According to American Col-
lege of Cardiology (ACC)/American Heart Association
(AHA) guidelines, thrombolytic therapy is indicated
up to 12 hours after onset of symptoms. It may even be
extended to 24 hours if the patients symptoms persist
or the chest pain is stuttering (waxing and waning)
and the ST segments remain elevated at the time of
entry. The thrombolytic agent should be infused
within 30 minutes after the patient enters the medical
facility on his own (door to needle time) or within 30
minutes after contact with emergency service person-
nel (medical contact to needle time).
The best results are obtained if the thrombolytic
agent is given within 1 to 2 hours after symptom on-
set because thrombolytic therapy is time dependent
and is more effective when given early.
The criteria for initiating a thrombolytic agent in a
patient with symptoms of acute ischemia are ST seg-
ment elevation or new (or presumably new) onset
left bundle branch block (LBBB).
n ST segment elevation:
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
C
D
n ST elevation 1 mm in any two or more adja-
cent precordial or limb leads.
n ST elevation is measured at the J point. The J
point is the junction between the terminal
portion of the QRS complex and beginning of
the ST segment. The preceding T-P segment
serves as baseline for measuring the ST eleva-
tion. The PR interval is used if the T-P seg-
ment is too short or is obscured by a U wave
or a P wave of sinus tachycardia.
n New-onset LBBB: The presence of LBBB will
mask the ECG changes of acute MI. If the LBBB
is new or presumably new and accompanied by
symptoms of acute myocardial ischemia, throm-
bolytic therapy is indicated.
Thrombolytic therapy is not indicated (and may be
contraindicated) in patients with acute ischemia asso-
ciated with ST depression or T wave inversion even if
the cardiac markers (troponins) are elevated.
The ECG is the most important modality not only in se-
lecting patients for thrombolytic therapy but also in mon-
itoring successful response to therapy. One of the earliest
signs of successful reperfusion during thrombolytic ther-
apy is relief of chest pain and resolution of the initial ST
segment elevation by at least 50% within 60 to 90 minutes
335
Figure 23.6: (Continued) (C) ST
Elevation MI. The above ECG was
recorded approximately 1.5 hours
from the initial ECG (see A).The ST
segments continued to evolve even
after thrombolytic therapy. ST eleva-
tion has become more pronounced
in V2 to V6 and slight elevation of the
ST segments is noted in II, III, and aVF.
Hyperacute T waves are still present
in V2 to V5 (arrows). (D) ST Elevation
MI. ECG recorded 13 days later. QS
complexes or decreased amplitude
of the r waves are seen in V1 to V5.
The ST segments are isoelectric and
the T waves are inverted from V16
and leads I, II, and aVL.
after initiation of therapy (Fig. 23.7). If ST segment reso-
lution does not occur within 90 minutes after initiating
thrombolytic therapy, rescue PCI should be considered.
Other signs of successful reperfusion include T wave
inversion occurring during the first hours of reperfu-
sion therapy and the presence of accelerated idioven-
tricular rhythm.
Primary Angioplasty
Primary PCI: Primary PCI requires immediate cardiac
catheterization and is the preferred method for revascu-
larizing patients with ST elevation MI (Fig. 23.8). The
ACC/AHA guidelines recommend that primary PCI
should be performed within 90 minutes after first med-
ical contact with emergency personnel (door to balloon
or medical contact to balloon) time. Unlike thromboly-
sis, it is more effective in reestablishing coronary blood
flow regardless of the duration of symptoms. It is the
preferred method in patients who are unstable, are he-
modynamically decompensated, when symptoms ex-
ceed 3 hours in duration or the diagnosis of ST eleva-
tion MI is in doubt.
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336 Chapter 23

Figure 23.7: ST Elevation My- A. Initial ECG

ocardial Infarction.
Electrocardiogram (ECG) A was
recorded before thrombolytic ther-
apy. ST segment elevation is present
in II, III, aVF, and V46 (arrows) with ST
depression in V12. (B) Taken 1 hour
after thrombolytic therapy. ST eleva-
tion in the inferolateral leads have
resolved and inverted T waves are
now present in lead III, both are signs
of successful reperfusion.
B. One hour after initial ECG

Figure 23.8:ST Elevation A. Initial ECG

Myocardial Infarction. Electro-
cardiogram (ECG) A shows ST eleva-
tion in V26, I and aVL (arrows). Coro-
nary angiography showed
completely occluded proximal left
anterior descending coronary artery.
ECG B was recorded 4 hours after
successful percutaneous coronary
intervention. The ST segment eleva-
tion has normalized without devel-
oping pathologic Q waves, a sign of
successful reperfusion.

B. After Percutaneous Coronary Intervention

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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 337

A B C D E F

Figure 23.9: ST Elevation. ST elevation MI may show different patterns in differ-

ent leads and may appear convex or coved (A, B), horizontal or plateau (C, D), oblique
(E), or concave (F) with a dart and dome configuration. Arrows point to the J points,
which are all elevated.

Because there is no standard limb lead representing

ST Elevation MI 60, aVL (30), which is closest to 60 and almost
directly opposite lead III, will show reciprocal ST
ST elevation MI generally indicates the presence of a depression (Figs. 23.11 and 23.12).
large infarct. The extent of the infarct is proportional to Similarly, if ST elevation is present in aVL, recipro-
the number of leads with ST segment elevation. ST el- cal ST depression will occur in lead III because lead
evation MI is associated with a lower ejection fraction, III is the closest lead directly opposite aVL.
higher incidence of heart failure, and a higher immedi- ST segment elevation always points to the area of in-
ate and in-hospital mortality when compared with jury. It is the primary abnormality even if reciprocal ST
non-ST elevation MI or unstable angina. depression is more pronounced than the ST elevation.
ST elevation MI may present with several ECG patterns
(Fig. 23.9). Although the characteristic example of ST el-
evation MI is an ST segment that is coved or convex up- Localizing the Infarct
ward (Fig. 23.9A,B), the ST elevation may be horizontal
or plateau (Fig. 23.9C,D), or it may be oblique, resem-
bling a ski-slope (Fig. 23.9E) or concave (Fig. 23.9F). The coronary arteries: Although variation in coronary
anatomy commonly occurs, three epicardial coronary
Tombstone pattern: Tombstoning is a type of ST
elevation MI where the ST segment is about the same
level as the height of the R wave and top of the T wave
(Figs. 23.4A and 23.6C). The QRS complex, ST seg- - 60o
ment, and T wave therefore blends together to form a
large monophasic complex similar to the shape of a
transmembrane action potential (Fig. 23.9C,D). Al-
though this pattern of ST elevation has been shown to
indicate a grave prognosis when compared with other
patterns of ST segment elevation, it is consistent with
the observation that the extent of muscle damage is
proportional to the magnitude of ST elevation. Tomb-
stoning is more commonly associated with acute ante-
rior MI. Involvement of the left anterior descending
coronary artery is usually proximal and is more severe
and extensive than when other patterns of ST eleva- o
III
tion are present. +120

Reciprocal ST depression: One of the features of ST

elevation MI that distinguishes it from other causes of
ST elevation is the presence of reciprocal ST depres-
sion. Reciprocal ST depression is the flip side image
recorded directly opposite the lead with ST elevation.
For example, if ST elevation occurs in lead III
(120), a flip side image will be recorded directly
opposite lead III at 60 (Fig. 23.10).
Figure 23.10: Reciprocal ST Depression. When ST
elevation from myocardial ischemia is recorded in any lead, a flip
side image is recorded directly opposite the lead. In the above
example, ST elevation is recorded in lead III (120), reciprocal ST
depression is also recorded at 60.Because there is no frontal lead
representing 60, lead aVL, which is adjacent to 60, will exhibit
the most pronounced reciprocal change (see Figs.23.11 and 23.12).
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338 Chapter 23
ECG Changes in ST Elevation MI
60o
aVR
aVL
30o
I Not all the areas of the heart are represented by the
III
II
+ 120o aVF
Figure 23.11: Reciprocal ST Depression. ST elevation in
lead III is associated with reciprocal ST depression directly oppo-
site lead III. Because lead aVL is the closest lead opposite lead III,
aVL will show the most pronounced reciprocal ST depression
among the standard electrocardiogram (ECG) leads.The
standard limb lead ECG is shown in Figure 23.12.
arteries are generally present. Each artery supplies specific
regional areas in the heart. These areas are topographi-
cally represented by the following groups of leads:
Left anterior descending (LAD) coronary ar-
tery: The LAD supplies the anterior, anteroseptal or
anterolateral wall of the left ventricle (LV) (leads
V1-V6, I, and aVL).
Right coronary artery (RCA): The RCA supplies
the inferior wall (leads II, III, and aVF), often pos-
terolateral wall of the LV (special leads V7, V8, V9).
The RCA is the only artery that supplies the right
ventricular free wall (special leads V3R to V6R).
Left circumflex (LCx) coronary artery: The LCx
supplies the anterolateral (leads I, aVL, V5, and V6)
and posterolateral (special leads V7, V8, V9) walls of
the LV. In 10% to 15% of patients, it supplies the in-
ferior wall of the LV (leads II, III, and aVF).
The following groups of leads represent certain areas of
the heart:
V12: ventricular septum.
V24: anterior wall of the LV. V2 overlaps the septum
and anterior wall and is both a septal and anterior lead.
V1-V3: anteroseptal wall of the LV.
V4-V6, I, and aVL: anterolateral wall of the LV.
V4-V6: lateral wall of the LV. V4 overlaps the anterior
and lateral walls of the LV and is both an anterior
and lateral lead.
V7-V9: (special leads) posterolateral wall of the LV.
V3R to V6R: (special right-sided precordial leads)
right ventricle.
I and aVL: basal anterolateral or high lateral wall of
the LV.
II, III, and aVF: inferior or diaphragmatic wall of the
LV.
12-lead ECG. The areas not represented include the
right ventricle and posterolateral wall of the LV. Special
leads V3R to V6R and V7 to V9 are needed to record these
areas, respectively. ST elevation involving the postero-
lateral wall of the LV is suspected when there is ST de-
pression in leads V1 to V3.
ST segment elevation points to the area of injury and is
helpful in identifying the infarct related artery. Acute
MI presenting as ST depression is frequently associated
with multivessel coronary disease and is less specific in
localizing the culprit vessel.
Myocardial Distribution of the
Three Main Coronary Arteries
The myocardial distribution of the three coronary ar-
teries is shown in Figure 23.13.
Left Anterior Descending
Coronary Artery
Anatomy: The left main coronary artery divides into
two large branches: the LAD and the LCx coronary
arteries. The LAD courses toward the apex through
the anterior interventricular groove and supplies the
anterior wall of the LV. The artery may continue to
the inferoapical wall by wrapping around the apex of
the LV (Fig. 23.14).
First branch: The first branch of the LAD is the first
diagonal artery. This branch runs parallel to the LCx
coronary artery and supplies the basal anterolateral
wall of the LV. If the first diagonal is a large branch,
complete occlusion of this artery causes ST eleva-
tion in leads I and aVL with reciprocal ST depres-
sion in III and aVF. These ECG changes may be in-
distinguishable from that due to occlusion of a small
LCx coronary artery.
Second branch: The second branch of the LAD is
the first septal branch. This artery may be the first
instead of the second branch. The artery penetrates
the ventricular septum perpendicularly and supplies
the basal septum including the proximal conduction
system. Involvement of the first septal perforator
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 339

will cause ST elevation in V1. It may also involve the

conduction system causing new onset right bundle
branch block.
Anterior MI: Depending on the location of the coro-
nary lesion and whether the LAD is large or small,
complete occlusion of the LAD will cause extensive an-
terior MI with varying degrees of ST elevation in V1 to
V6 as well as leads I and aVL.
Before the first branch: If the LAD is occluded
proximally at the ostium or before the first branch
(first diagonal), ST elevation will occur in V1 to V4
(or up to V6) and leads I and aVL from extensive an-
terior MI. The ST elevation in leads I and AVL rep-
resent involvement of the first diagonal branch and Figure 23.12: Reciprocal ST Depression. ST elevation is
is usually accompanied by reciprocal ST depression present in leads II, III, and aVF and is most marked in lead III
in III and aVF (Figs. 23.15 and 23.16). (arrows). Reciprocal ST depression is most pronounced in aVL
Between the first and second branches: If the (double arrows) because aVL is almost directly opposite lead III
lesion is distal to the first diagonal (but proximal to (see Fig. 23.11).
the first septal branch), ST elevation will include V1
to V4 but not leads I and aVL consistent with acute
anteroseptal MI. ST elevation in V1 indicates in- Occlusion of the first diagonal branch: If a
volvement of the first septal branch (Fig. 23.17). large first diagonal branch is the only artery oc-
After the second branch: If the lesion is distal to cluded, and the LAD is spared, ST elevation is
the first diagonal and first septal branches, ST eleva- confined to leads I and aVL consistent with high
tion will involve V2-V4 but not V1 or I and aVL con- lateral MI, which involves the base of the LV (Fig.
sistent with anterior often called apical MI. 23.18).

LAD LCx RCA Figure 23.13: Myocardial Distribu-

tion of the Coronary Arteries. The
diagrams summarize the myocardial dis-
Anterior tribution of the three coronary arteries.
LAD artery
PA Right The diagram in the upper left represents
LA 1 Ventricle Anterior
LV Wall the frontal view of the heart. The left
RA Ao Right Left ventricle is transected by three lines
MV
Posterior labeled 1, 2, and 3. Line 1 is at the level of
Descending the mitral valve which corresponds to the
LV
V1 V2 Artery
base of the left ventricle. The short axis
Lateral LV wall
view is shown on the upper right
RV V3
Posterior diagram. Line 2 corresponds to the mid-
V4 V5 V6 ventricle and the short axis is shown at
the lower left. Line 3 corresponds to the
apex of the left ventricle and the short
2 axis is shown at the lower right. Ao, Aorta;
Anterior
LAD artery LA, left atrium; LV, left ventricle; LAD, left
RV Anterior
3 anterior descending; LCx, left circumflex;
Anterior
LV Wall
LV, left ventricle; MV, mitral valve; PA, pul-
Right Left
LV monary artery; PDA, posterior descend-
Anterolateral
PDA
PM Right LV Left ing artery; PM, papillary muscle; RA, right
Posteromedial atrium; RCA, right coronary artery; V1 to
PM Lateral LV wall
LCx Artery V6, the precordial electrodes
Inferior LV wall = RCA
superimposed on the heart.
Posterior
Posterior

2: Short Axis, LV Papillary Muscle 3: Short Axis, LV Apex

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340 Chapter 23

Figure 23.14: Diagrammatic Aorta

Representation of the LAD and its
Left Main Coronary Artery
Branches. The left main coronary artery LA
RA
divides into two main branches: the LAD
LCx Coronary Artery
and LCx coronary arteries.The LAD courses LAD
First Diagonal Branch
through the anterior interventricular First Septal
groove. It gives diagonal branches laterally Branch RV LV
Diagonal
and septal branches directly perpendicular Branches
Septal Branches
to the interventricular septum. LA, left
atrium; LAD, left anterior descending artery;
LCx, left circumflex; LV, left ventricle; RA, right
atrium; RV, right ventricle.
Anterior Surface

Figure 23.15: Extensive Anterior Myocardial Infarction (MI). ST elevation is present

in leads V16, I, and aVL. Cardiac catheterization showed complete occlusion of the proximal left
anterior descending (LAD) artery. Note that the ST elevation in I and aVL is due to involvement
of the first diagonal branch, which is usually the first branch of the LAD. ST depression in II, III,
and aVF is a reciprocal change due to ST elevation in I and aVL.

Figure 23.16: Extensive Anterior Myocardial Infarction. ST elevation is present in

V16, I, and aVL. Coronary angiography showed complete occlusion of the proximal LAD. This
electrocardiogram is similar to that in Figure 23.15.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 341

Figure 23.17: Left Anterior

Descending (LAD) Artery Oc-
clusion Distal to the First Di-
agonal Branch. The electrocar-
diogram shows acute anteroseptal
myocardial infarction with ST seg-
ment elevation confined to V1 to
V4. This is due to occlusion of the
LAD distal to the first diagonal
branch (no ST elevation in I and
aVL) but proximal to the first sep-
tal branch (ST elevation is present
in V1).

eventually Q waves not only in the anterior wall but

LAD Coronary Artery also inferiorly in II, III, and aVF (Fig. 23.19).

Two ECGs showing anterior MI from occlusion of the

LAD. The first ECG in Figure 23.16 shows ST elevation
in I and aVL from occlusion of the LAD before the first
diagonal branch. The second ECG in Figure 23.17 shows
anterior MI without ST elevation in I and aVL because
of occlusion of the LAD after the first diagonal branch.
Figure 23.18 shows occlusion confined to the first diago-
nal branch of the LAD, resulting in high lateral wall MI.
ST elevation is present in leads I and aVL only. The ST
segment depression in leads III and aVF are reciprocal
changes due to the elevated ST segments in I and aVL.
If the LAD is a long artery, it may wrap around the apex
and continues to the inferoapical wall of the LV. Occlu-
sion of a wrap around LAD may cause ST elevation and
LCx Artery
Anatomy: The LCx coronary artery circles the left atri-
oventricular (AV) groove laterally between the left
atrium and LV and gives branches that supply the an-
terolateral and posterolateral walls of the LV (Fig.
23.20). The artery may be small and may terminate
very early. In 10% to 15% of cases, the LCx continues
posteriorly toward the crux of the heart and down the
posterior interventricular groove as the posterior de-
scending coronary artery. When this occurs, the LCx is
the dominant artery and supplies not only the inferior

Figure 23.18: Acute High Lateral Myocardial Infarction from Isolated Lesion
Involving the First Diagonal Branch of the Left Anterior Descending (LAD)
Artery. ST segment elevation is confined to leads I and aVL. Coronary angiography showed
complete occlusion of the first diagonal branch of the LAD. The LAD itself is patent. Occlusion
of the first diagonal branch of the LAD causes ST elevation in I and aVL with reciprocal ST
depression in III and aVF.
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342 Chapter 23

Figure 23.19: Anterior and Inferior Myocardial Infarction. QS complexes with ST ele-
vation is noted in V1 to V5 (anterior wall) and also in leads II, III, and aVF (inferior wall) due to an
occluded left anterior descending artery that wraps around the apex of the left ventricle
extending to the inferoapical left ventricular wall. The right coronary artery is small but patent.

wall of the LV but also gives rise to the artery to the AV
node. Occlusion of the LCx artery will cause:
Anterolateral MI: When the LCx coronary artery is
occluded proximally, ST elevation will occur in leads
I, aVL, V5, and V6. The MI is confined to the area
bounded by the two papillary muscles posterolater-
ally from the base to the proximal two thirds of the
LV (Fig. 23.21). The ST elevation may occur only in
leads I and aVL and may be difficult to differentiate
from an occluded first diagonal branch of the LAD
(Figs. 23.18 and 23.22).
Posterolateral MI: The posterolateral wall of the
LV is not directly represented by any standard ECG
lead. When posterolateral MI occurs, reciprocal ST
depression is noted in V1-V3. V5, and V6 may show
ST elevation (Fig. 23.23).
Aorta
LCx
Coronary Left Anterior Descending
Artery
MA TA
Left Atrioventricular Branch
Posterior Descending
Obtuse
Marginal Artery (10-15%)
Branches LV RV
Posterolateral
Branches
Posterior View of the Heart
Figure 23.20: Left Circumflex (LCx) Coronary Artery.
The diagram represents the LCx artery and its main branches. In
10% to 15% of patients, the LCx artery is the dominant artery by
continuing as the posterior descending artery (dotted lines) and
supplying the artery to the AV node. LV, left ventricle; MA, mitral
annulus; RV, right ventricle; TA, tricuspid annulus.
The myocardial distribution of the LCx coronary artery
is shown in Fig. 23.21. Acute MI from occlusion of the
LCx coronary artery is shown in the ECG in Figure 23.22.
Posterolateral MI: Occlusion of the LCx artery can
cause posterior, straight posterior, or posterolateral MI.
Because there are no leads representing the posterolat-
eral wall of the LV, a posterolateral MI is suspected in
the 12-lead ECG when there is ST depression in V1 to
V3. These leads are directly opposite the posterolateral
wall and will show reciprocal ST depression when a pos-
terior MI is present. Posterior MI can be confirmed by
placing extra electrodes in V7, V8, and V9 (V7 is located
at the left posterior axillary line, V8 at the tip of the left
scapula, and V9 at the left of the spinal column in the
same horizontal plane as V46). These special leads will
show Q waves with ST elevation if a posterolateral MI is
present. Prominent R waves may or may not be present
in the anterior precordial leads (Fig. 23.23).
Although ST depression is not an indication for
thrombolytic therapy, ST depression in V1 to V3 may
be due to posterior MI, which represents a true ST
elevation MI. Before thrombolytic therapy is given,
leads V79 should be recorded to verify that the ST de-
pression in V13 is due to posterior MI and not from
subendocardial injury involving the anterior wall of
the LV.
ST elevation confined to leads I and aVL usually indi-
cate lateral MI due to involvement of the LCx coronary
artery (Fig. 23.24). ST elevation in leads I, aVL, V5, and
V6 is often accompanied by ST elevation in V7 to V9 and
reciprocal ST depression in V1 to V3 from posterolat-
eral MI. ST elevation in V6 is usually accompanied by
ST elevation in V7 to V9 because these leads are adjacent
to V6 (Figs. 23.25 and 23.26).
Figure 23.26 shows the importance of recording special
leads V7 to V9 when a posterolateral MI is suspected.
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L CX LAD RCA
Anterior
Anterior
RV
LAD artery
Ao
RV Anterior Right LV Left
LV LV Wall
Right
LA LV Left
Postero
Postero Posterior
10-15% lateral
Medial PM
LV wall 10-15%
LCx

A: Long Axis B: Short Axis (Level of PM) C: Short Axis (Apex)

Figure 23.21: Myocardial Distribution of the Left Circumflex (LCx) Coronary Artery. The LCx coro-
nary artery supplies the territory represented by the purple checkered lines. These include the proximal two
thirds (base and midportion) of the lateral wall of the left ventricle. In 10% to 15% of patients, the LCx is the domi-
nant artery and continues inferiorly to the apex of the left ventricle as the posterior descending coronary artery
(A) long axis view. (C) Short axis view of the apex. Ao, aorta; LA, left atrium; LAD; left anterior descending coronary
artery; LCx, left circumflex; LV, left ventricle; PM, papillary muscle; RV, right ventricle.

Figure 23.22: High Lateral My-

ocardial Infarction (MI). Q waves
with elevation of the ST segments
are confined to leads I and aVL. The
ST depression in III and aVF is recip-
rocal to the ST elevation in I and aVL.
This represents high lateral MI result-
ing from occlusion of the left circum-
flex coronary artery. This electrocar-
diogram finding can also occur when
there is occlusion of the first diagonal
branch of the left anterior descend-
ing coronary artery (see Fig. 23.18).

Figure 23.23: Acute Posterolateral Myocardial Infarction (MI). There is marked

depression of the ST segments in V1 to V3 with tall R waves in V12. The amplitude of the R
waves in V56 is diminished and the ST segments are elevated. This represents an acute pos-
terolateral MI from an occluded left circumflex coronary artery. The ST depression and tall R
waves in V1-V3 are reciprocal changes due to the posterior MI. Anterior subendocardial injury
and straight posterior MI can be differentiated by recording V79, which will show ST
elevation if posterior MI is present. This distinction is important because ST elevation MI in-
volving the posterior wall of the left ventricle may require thrombolysis, whereas anterior
wall subendocardial injury does not.

343
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344 Chapter 23

Figure 23.24: Acute High

Lateral Myocardial Infarction.
ST segment elevation is noted in I
and aVL with reciprocal ST
depression in III and aVF from occlu-
sion of the left circumflex coronary
artery. The ST depression in II, III, and
aVF is reciprocal to the ST elevation
in I and aVL.

The standard 12-lead ECG shows ST depression in V1 Right Coronary Artery

to V3 and ST elevation in V5 and V6. Special leads V7 to
V9 recorded posteriorly shows Q waves with ST seg-
ment elevation similar to V6. These changes are consis-
tent with a transmural posterolateral MI. The coronary
angiogram confirmed the presence of a completely oc-
cluded LCx artery.
Inferior MI: Acute inferior MI is due to occlusion of
the RCA in 85% to 90% of patients but it can occur in
10% to 15% of patients when the LCx is the dominant
artery. In acute inferior MI, the ST segments are ele-
vated in II, III, aVF. If the LCx is the culprit vessel, the
ST elevation in lead II is greater than or equal to the ST
elevation in lead III (Fig. 23.27).
If the LCx is small and nondominant, occlusion of the
artery may not show any ECG changes (Fig. 23.28).
Thus, a normal ECG does not exclude acute MI espe-
cially when the LCx is the culprit vessel because most of
the area supplied by the LCx is not represented in the
standard 12-lead ECG.
Anatomy: The RCA courses around the medial AV
groove between the right atrium and right ventricle and
supplies acute marginal branches to the right ventricle. In
85% to 90% of cases, it is the dominant artery in that it
gives rise to the artery to the AV node before continuing
posteriorly toward the apex of the LV as the posterior de-
scending artery, which supplies the inferior wall of the LV.
The artery often continues posterolaterally beyond the
crux to the opposite (lateral or left) AV groove and sends
posterolateral branches to the LV (Fig. 23.29).
Total occlusion of the RCA will cause the following
ECG changes:
Inferior MI: ST elevation in leads II, III, and aVF with
reciprocal ST depression in I and aVL (Fig. 23.30).
Inferolateral MI: ST elevation in leads II, III, aVF, V5,
and V6. ST elevation in V5-V6 suggests that the lateral
wall of the LV is also involved (Figs. 23.31 and 23.32).

Figure 23.25: Acute Posterolateral Myocardial Infarction (MI). ST depression is

present in V1-V4.These changes can represent subendocardial injury involving the anterior
wall or ST elevation MI involving the posterior wall of the left ventricle. The presence of ST
elevation in V6, I, and aVL favors acute posterolateral MI rather than anterior wall injury. This
can be confirmed by recording V79, which will show ST elevation if posterior MI is present.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 345

A: Standard 12 lead ECG Figure 23.26: Posterolateral

Myocardial Infarction (MI) and
Special Leads V79. Electrocardio-
gram (ECG) A is a 12-lead ECG of a 58-
year-old male presenting with chest
pain. There is ST elevation in leads I,
V5, and V6, and ST depression in V13.
(B) The same as ECG A and shows
only the precordial leads together
with V7 to V9. ST elevation is present
in V6 as well as V7, V8, and V9
consistent with acute posterolateral
MI. These examples show the impor-
B: Precordial leads V1 to V9
tance of recording special leads V7 to
V1 V4 V7 V9 in confirming the diagnosis of pos-
terolateral MI. ECG courtesy of Kittane
Vishnupriya, MD.

V2 V5 V8

V3 V6

Inferoposterior MI: ST elevation in leads II, III,
and aVF with ST depression in V1 to V3. Recipro-
cal ST depression in V1-V3 indicates the presence
of a posterolateral MI (Figs. 23.33 and 23.34). Tall
R waves may develop in V1 or V2, although this
usually occurs much later several hours after the
acute episode. Special leads V79 will record ST el-
evation and tall hyperacute T waves during the
acute episode.
ST depression in V1-V3 may be due to ST elevation MI
involving the posterolateral wall (Figs. 23.33A and
23.34). It may also be due to subendocardial injury in-
volving the anterior wall of the LV. To differentiate one
from the other, leads V7 to V9 should be recorded. If
posterolateral ST elevation MI is present, V7 to V9 will
record ST segment elevation. If there is subendocardial
injury involving the anterior wall, the ST segments will
not be elevated in V7 to V9.

Figure 23.27: Acute Inferior Myocardial Infarction (MI) from Occlusion of the
Left Circumflex Coronary Artery. Note that the ST elevation in lead II is more prominent
than lead III. Additionally, the ST segment is isoelectric in aVL and minimally elevated in lead I.
ST depression is present in V1 to V3 with ST elevation in V6 from posterolateral MI.
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346 Chapter 23

Figure 23.28: Acute Myocardial Infarction with Normal Electrocardiogram (ECG).

The ECG is from a 56-year-old male who presented with acute persistent chest pains. Serial ECGs
were all normal although the cardiac markers were elevated. The coronary angiogram
showed completely occluded left circumplex corona artery (LCx). Among the three coronary
arteries, LCx coronary disease is the most difficult to diagnose electrocardiographically.

possible only when the proximal RCA is occluded. It

Acute Inferior MI is diagnosed by the presence of ST elevation 1 mm
in any of the right sided precordial leads V3R to V6R,
Inferior MI: In 85% to 90% of patients with acute infe- with lead V4R the most sensitive (Fig. 23.35). If right-
rior MI, the culprit vessel is the RCA and in the re- sided precordial leads were not recorded, V1 should be
maining 10% to 15%, the LCx coronary artery. Inferior examined for ST segment elevation. Occlusion of the
MI can also occur when a long LAD that goes around LCx will not result in RVMI because the LCx circles
the apex of the LV is occluded resulting in anterior MI the lateral AV groove and does not supply branches to
that extends to the inferoapical wall (Fig. 23.19). the right ventricle (diagram in Fig. 23.20).
RCA and inferior MI: The following ECG findings in- ST elevation in lead III  II: When the RCA is to-
dicate that the RCA is the culprit vessel when inferior tally occluded, the highest ST elevation will be
MI is present. recorded in lead III (Fig. 23.36). This is based on the
Right ventricular MI (RVMI): The presence of anatomical location of the RCA, which circles the
RVMI always indicates RCA involvement. RVMI is right AV groove, and is closer to lead III than lead II
in the frontal plane. This is in contrast to the LCx
coronary artery, which is closer to lead II than lead
III because it circles the left or lateral AV groove.
Aorta Reciprocal ST depression in aVL  lead I: Be-
cause lead III has the highest ST elevation when the
Right Coronary Artery
RCA is occluded, the most pronounced ST depres-
Right Acute Marginal
sion will be recorded opposite lead III at 60. Be-
MA TA
atrioventricular Branches cause aVL (at 30) is adjacent to 60, aVL will
branch record the deepest reciprocal ST depression if the
RCA is the culprit vessel.
Posterolateral RV
branches Posterior Descending
LCx and inferior MI: If a dominant LCx is the cause of
LV
Artery the inferior MI, ST elevation in lead III is not taller
than lead II and the ST segments are isoelectric (or may
Posterior View of the Heart be elevated) in aVL and lead I as shown in Figure 23.27.
ST elevation in leads II, III, and aVF with ST depression
Figure 23.29: Diagrammatic Representation of a Dom- in V2 and V3 also favors a LCx lesion since the LCx sup-
inant Right Coronary Artery (RCA). The RCA continues plies posterolateral branches to the LV, which is dia-
posteriorly as the posterior descending artery and often goes metrically opposite V2 and V3. However, if the LCx is
beyond the crux to supply posterolateral branches to the left small and the RCA is the dominant artery, the RCA
ventricle (dotted lines). LV, left ventricle; MA, mitral annulus; RV, may continue beyond the crux to the left AV groove to
right ventricle; TA, tricuspid annulus. supply posterolateral branches to the LV.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 347

Figure 23.30: Acute Inferior

Myocardial Infarction (MI). ST
segment elevation is present in II, III,
and aVF with reciprocal ST
depression in I and aVL consistent
with acute inferior MI. This is due to
occlusion of the right coronary
artery.

Figure 23.31: Acute

Inferolateral Myocardial Infarc-
tion. The ST segments are elevated
in leads II, III, and aVF with reciprocal
ST depression in aVL. ST segments
are elevated in V5 and V6 with ST seg-
ment depression in V1 and V2. Coro-
nary angiography showed complete
occlusion of the proximal right coro-
nary artery.

Figure 23.32: Acute Inferolat-

eral Myocardial Infarction. ST
elevation is noted in II, III, aVF, and V4
to V6 with reciprocal ST depression in
I and aVL.The findings are similar to
those in Figure 23.31.

A B 60 Figure 23.33: Posterolateral Myocardial Infarc-

aVR
aVL
tion (MI). Posterolateral MI is a true ST segment ele-
V1 V2 30 vation MI. This is suspected when there is ST segment
V3
I depression in V13 (A). The ST depression in V13 is a
R V6 L reciprocal pattern due to ST elevation in the posterolat-
eral wall similar to the reciprocal pattern seen in aVL
III
when there is ST elevation in lead III (B). Posterolateral
Posterolateral V8 II
MI +120 aVF MI can be verified by recording special leads V79, which
V9
will confirm the presence of ST elevation in this area.
Posterior
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348 Chapter 23

Figure 23.34: Acute Inferopos-

terior Myocardial Infarction
(MI). ST segments are elevated in II,
III, and aVF with reciprocal ST depres-
sion in leads I and aVL consistent
with an acute inferior MI.There is also
ST depression in V1 to V4 and ST ele-
vation in V6 from posterolateral MI.
The P waves (arrows) are completely
dissociated from the QRS complexes
because of AV block.

V3R
V3
V4R
V4
V5R V5
V1 V2

V6R V6

Figure 23.35: Right-Sided Precordial Leads. The right-

sided precordial leads are labeled V3R to V6R (open circles).The
leads are obtained by repositioning the standard precordial
electrodes V36 (dark circles) to the right side of the chest. Leads
V1 and V2 remain in their original location.

Figure 23.36: Acute Inferior Myocardial Infarction (MI). The 12-lead electrocardio-
gram shows ST segment elevation in II, III, and aVF with reciprocal ST depression in I and aVL
from acute inferior MI. There is also reciprocal ST depression in V2 and V3 from involvement of
the posterior wall of the left ventricle. Note that the ST elevation in lead III is higher than the ST
elevation in lead II and ST depression in aVL is deeper than the ST depression in I, suggesting
that the culprit vessel is the right coronary artery. The right-sided precordial leads are shown.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 349

V2 V4R

V5R
V1

V3R V6R

Figure 23.37: Acute Inferior MI with Right Ventricular Myocardial Infarction

(RVMI). The diagnosis of RVMI is based on the presence of 1 mm ST elevation in any of
the right sided precordial leads V3R to V6R (arrows). The electrocardiogram shows at least 1
mm of ST elevation in V4R, V5R, and V6R consistent with RVMI. It is not necessary to switch V1
and V2, as was done above when recording right-sided precordial leads. The presence of
RVMI suggests that the culprit vessel is the proximal right coronary artery.

not routinely recorded if there is no evidence of acute

Right Ventricular Myocardial Infarction
RVMI: RVMI is a common complication of acute infe-
rior MI. If the initial ECG confirms the diagnosis of
acute inferior MI, right-sided precordial leads should be
recorded immediately (Fig. 23.37). This is a Class I indi-
cation according to the 2004 ACC/AHA guidelines on
ST elevation MI. If right-sided precordial leads are not
immediately recorded, ST elevation in the right precor-
dial leads may disappear within 10 hours after symptom
onset in approximately half of patients with RVMI.
Right sided precordial leads are recorded by reposition-
ing the precordial leads V3, V4, V5, and V6 to the right
side of the chest in the same standard location as that
on the left (Fig. 23.35). Right-sided precordial leads are
inferior MI.
Any ST elevation 1 mm in any of the right sided pre-
cordial leads V3R to V6R is consistent with RVMI. These
leads, especially V4R, are the most sensitive and most
specific for the diagnosis of RVMI.
RVMI is possible only when the proximal RCA is oc-
cluded. It does not occur when the distal RCA or LCx
coronary artery is involved. This is important prognosti-
cally because occlusion of the proximal RCA usually im-
plies the presence of a larger infarct and is associated
with a high incidence of AV nodal block when compared
to occlusion of a nondominant LCx or distal RCA.
RVMI: Very often, right-sided precordial leads are not
recorded at the time of entry. These leads are special
leads and are not routine in a regular 12-lead ECG.

Figure 23.38: Right Ventricular

Myocardial Infarction (RVMI).
The diagnosis of RVMI should always
be suspected in the standard 12-lead
electrocardiogram when acute infe-
rior MI is present. ST elevation in lead
III greater than lead II and presence
of ST elevation in V1 indicate RVMI as
shown above. If the ST elevation in V1
extends to V2 or V3, it may resemble
acute anterior MI.
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350 Chapter 23

RCA Anterior
RV Anterior
RCA
Ao RV
LV LV
Right apex Left
LA Left
Right
LV
Postero
Antero-
Medial PM Posterior RCA
Lateral wall lateral PM

A: Long Axis B: Short Axis (Level of PM) C: Short Axis (Level of Apex)
D

Figure 23.39: (A) Myocardial Distribution of the Right Coronary Artery (RCA).
The red stippled areas represent myocardial distribution of the RCA.These include the right
ventricular free wall, lower one-third of the posterolateral wall (A, B), inferior half of the ven-
tricular septum (B) and the posterior portion of the LV apex (C). Note that the posteromedial
PM (B) is supplied only by the RCA, whereas the anterolateral PM is supplied by two arteries,
the LAD and LCx. Ao, aorta; LA, left atrium; LAD, left anterior descending; LCx, left circumflex;
LV, left ventricle; PM, papillary muscle; RV, right ventricle. (D) Electrocardiogram (ECG) of
RCA Involvement. Twelve-lead ECG showing a proximally occluded RCA.There is inferior my-
ocardial infarction (MI) with ST elevation in lead III taller than lead II and ST depression in aVL
more pronounced than lead I. Even when right sided precordial leads are not recorded, the
presence of right ventricular MI can be diagnosed by the ST elevation in V1.

Even if they were recorded, they may be recorded much
later and not within the limited time window in which
RVMI can be diagnosed. RVMI can be suspected if the
initial standard 12-lead ECG will show the following
changes:
ST elevation in lead III is greater than lead II:
This suggests that the RCA (and not the LCx), is the
cause of the inferior MI (Figs. 23.30, 23.38, and
23.39B).
ST elevation is present in V1 (Figs. 23.30 and
23.38): Although V1 is not a very sensitive lead for
the diagnosis of RVMI when compared with V4R, V1
is also a right-sided precordial lead. Thus, ST eleva-
tion in V1 during acute inferior MI may be the only
indication that an RVMI is present if right-sided
precordial leads were not recorded in the ECG. The
ST elevation may extend to V3 resembling anterior
MI (Fig. 23.38).
Conversely, RVMI is not possible if the LCx coronary
artery is the culprit vessel. If the LCx artery is the cul-
prit vessel, ST elevation in III is not greater than lead II.
ST depression is not present in aVL and ST elevation
may be present in lead I (Fig. 23.27).
The myocardial distribution of the RCA is summarized
in Figures 23.39A-C. The RCA is the dominant artery
when it is the origin of the posterior descending coro-
nary artery. This occurs in 85% to 90% of all patients.
It supplies the whole inferior wall from base to apex
and is the only artery that supplies the right ventricular
free wall (Fig. 23.39A).
Figures 23.39D shows the ECG of a patient with oc-
cluded proximal RCA. The presence of RVMI can be
recognized even when the right-sided precordial leads
are not recorded.
Complications of Acute MI
The ECG can provide very useful information not only
in correctly identifying the culprit coronary artery but
also in predicting possible complications based on the
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 351

TABLE 23.1

ST Elevation, MI Location, and Possible Complications

Leads with
ST Elevation Location of the MI Infarct-Related Artery Possible Complications
II, III, aVF Inferior wall of the RCA in 85% to 90% RCA  VT/VF, RVMI, bradyarrhythmias
left ventricle including sinus bradycardia, hypoten-
sion and AV block, LV dysfunction,
postero-medial papillary muscle
dysfunction, or rupture
LCx in 10% to 15% Dominant LCx: VT/VF, LV dysfunction,
AV block but no RVMI or papillary
muscle dysfunction
I and aVL High lateral LCx or first diagonal VT/VF, LV dysfunction
branch of LAD
V1V4 Anteroseptal LAD VT-VF, extensive LV dysfunction, RBBB 
fascicular block, cardiogenic shock
V5V6  I, aVL Lateral LCx VT/VF, LV dysfunction
ST depression in Posterior or LCx , RCA also possible VT/VF, LV dysfunction
V1V3  tall R waves straight posterior
II, III, aVF  RVMI Proximal RCA VT/VF, AV block, bradycardia, hypotension,
V3R, V4R, or V5R atrial infarction
AV, atrioventricular; LAD, left anterior descending; LCx, left circumflex; LV, left ventricular; PM, papillary muscle; RBBB, right bundle branch block;
RCA, right coronary artery; RVMI, right ventricular MI; VT/VF, ventricular tachycardia/ventricular fibrillation.

geographic location of the acute MI. Table 23.1 identi-
fies the location of the MI based on the leads with ST
elevation, identifies the infarct related artery, and the
possible complications associated with the MI.
Ventricular tachycardia (VT) or ventricular fibrilla-
tion (VF): Most deaths from acute MI occur suddenly
usually during the first hour after onset of symptoms due
to VF (Fig. 23.40). More than half of these deaths occur
even before the patient is able to reach a medical facility.
Sustained VT or VF within the first 48 hours: In-
hospital mortality is increased among patients with
acute MI who develop VT/VF. Survivors of VT/VF
occurring within 48 hours after onset of acute MI
have the same long-term prognosis compared with a
similar group of patients without VT/VF. In these
patients, VT/VF is due to electrical instability associ-
ated with acute myocardial injury, which may re-
solve after the acute injury has subsided.

Figure 23.40: Ventricular Fibrillation. This rhythm strip was obtained from a 54-year-
old male with ST elevation myocardial infarction. His initial electrocardiogram is shown in
Figure 23.18. He developed ventricular fibrillation while he was being monitored in the emer-
gency department. His timely arrival to the hospital allowed him to be resuscitated success-
fully. The coronary angiogram showed total occlusion of the first diagonal branch of the left
anterior descending artery, which was successfully stented. He left the hospital without neu-
rologic sequelae and only minimal myocardial damage.
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352 Chapter 23

Figure 23.41: Accelerated A.

Idioventricular Rhythm. The
12-lead electrocardiogram (ECG) in
A shows normal sinus rhythm and
acute inferior MI. (B) The same
patient a few minutes after ECG A
was recorded, showing accelerated
idioventricular rhythm.

B.

Sustained VT or VF after 48 hours: Survivors of
cardiac arrest due to VT/VF occurring after 48 hours
of acute MI continue to be at risk for VT/VF. Unless
the arrhythmia has been shown to be due to elec-
trolyte abnormalities or due to recurrent acute is-
chemia, which are reversible, these patients are at
high risk for developing recurrence of VT/VF and
will benefit from implantation of an automatic de-
fibrillator even without electrophysiologic testing.
One of the most important factors that determine the
prognosis of patients with acute MI is the extent of my-
ocardial damage. The presence of severe myocardial
damage and a low left ventricular ejection fraction pre-
disposes to ventricular arrhythmias, which may cause
sudden death.
Other ventricular arrhythmias: Some arrhythmias
may be related to reperfusion after successful throm-
bolysis and should be recognized. The most frequent
ECG finding associated with successful reperfusion is
accelerated idioventricular rhythm (AIVR).
AIVR: AIVR is a ventricular rhythm with a rate of 60 to
110 beats per minute (bpm). AIVR commonly occurs
as a reperfusion arrhythmia and is more commonly
seen after thrombolysis rather than with primary PCI.
It occurs with about equal frequency in patients with
acute inferior (Fig. 23.41) and anterior MI (Fig. 23.42).
The arrhythmia is generally benign and does not re-
quire any therapy.
AIVR may be difficult to recognize and may be mis-
taken for ventricular tachycardia or new onset bundle
branch block (Fig. 23.42). In AIVR, the QRS complexes
are not preceded by P waves or there is complete AV
dissociation. This may result in decreased cardiac out-
put because atrial contraction no longer contributes to
left ventricular filling.
Acute inferior MI and AV block: When acute inferior
MI causes AV block, the AV block is at the level of the
AV node (Figs. 23.43 and 23.44).
Acute MI and Right Bundle Branch
Block (RBBB)
Among 26,003 patients with acute MI studied in
GUSTO-1 (Global Utilization of Streptokinase and tPA
for Occluded Coronary Arteries), 289 patients (1.1%)
had RBBB. Most of these patients with RBBB had ante-
rior MI. In 133 patients, only RBBB was present. In 145
patients, left anterior fascicular block was also present.
Only 11 patients had RBBB with left posterior fascicular
block.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 353

A. Figure 23.42: Accelerated

Idioventricular Rhythm. Electro-
cardiogram (ECG) A shows normal
sinus rhythm with acute anterosep-
tal MI. ECG B shows a sudden change
in the configuration of the QRS com-
plexes with tall R waves in V1 and a
rightward shift in the axis of the QRS
complex in the frontal plane due to
accelerated idioventricular rhythm.
This ECG can be mistaken for new-
onset right bundle branch block
with left posterior fascicular block.

B.

Figure 23.43: Acute Inferior Myocardial Infarction (MI) and Complete

Atrioventricular (AV) Block. The P waves (arrows) and QRS complexes are completely
dissociated consistent with complete AV block. When complete AV block occurs in the
setting of an acute inferior MI, the AV block is at the level of the AV node. The AV block is usu-
ally reversible and permanent pacing is usually not indicated.
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354 Chapter 23

Figure 23.44: Acute Inferolat-

eral Myocardial Infarction with
2:1 Atrioventricular (AV) Block.
The electrocardiogram shows 2:1 AV
block. The arrows identify the
second P wave that is not
conducted.

Changes in the ST segment and T wave when
there is (RBBB): The diagnosis of acute MI is not diffi-
cult when there is RBBB. Changes in the Q waves, ST
segment, and T waves continue to be useful.
RBBB without MI: In RBBB without MI, the ST
segments and T waves are normally discordant (op-
posite in direction) in relation to the terminal por-
tion of the QRS complex. Thus, in V1, the T waves
are normally inverted and the ST segments are de-
pressed because terminal R waves are present when
there is RBBB. In V6, the T waves are upright and the
ST segments are elevated since terminal S waves are
present (Figs. 23.45A and 23.46).
RBBB with acute MI: When ST elevation MI is
complicated by RBBB, the ST segments become
concordant (same direction) in relation to the ter-
minal portion of the QRS complex. Thus, in ante-
rior MI, the ST segments are elevated in V1 and of-
ten in V2 because terminal R waves are normally
present in these leads. Similar concordant changes
may be noted in leads II, III, and aVF when there is
inferior MI (Figs. 23.47 and 23.48B).
Two examples of RBBB are shown in Figure 23.46, in
which the RBBB is uncomplicated without evidence
of MI. Note the presence of normally discordant ST
segments and T waves. The second patient has inferior
MI complicated by RBBB (Fig. 23.47). Note the pres-
ence of concordant ST elevation in leads III, aVF, and
V1, and concordant ST depression in leads I, aVL, and
V2.
Q wave changes: RBBB does not interfere with the di-
agnosis of acute ST elevation MI. Changes in the

S wave
down
V1 ST and T
V6 V1 V6
S wave down ST and T
wave down wave also
down

ST and T
R wave up
wave up
R wave up
ST and T wave
are also up

A: Uncomplicated RBBB B: RBBB with MI

Figure 23.45: ST-T Changes in Right Bundle Branch Block (RBBB). (A) In uncompli-
cated RBBB, the ST segment and T wave are normally discordant (opposite in direction) to the
terminal portion of the QRS complex. (B) When ST elevation myocardial infarction occurs, the ST
segment (and T wave) becomes concordant (same direction) in relation to the terminal portion
of the QRS complex.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 355

A. RBBB without MI
Terminal R

ST and T wave discordant

ST and T wave discordant

S wave

Figure 23.46: Right Bundle Branch Block (RBBB) without Myocardial

Infarction. In uncomplicated RBBB without ST elevation MI, the ST segments and T waves
are normally discordant.Thus, the ST segments and T waves are inverted in V1 because the
QRS complex ends with a terminal R wave. In leads I and II, the ST segments are normally el-
evated and T waves are upright because the QRS complex ends with an S wave. These ST-T
abnormalities are secondary to the presence of RBBB.

Q waves or QRS complexes remain useful and can be
used for diagnosis. This is unlike LBBB, where the QRS
complexes are significantly altered by the conduction
abnormality making diagnosis of ST elevation MI by
ECG extremely difficult.
Anterior MI and AV Block
Acute anterior MI can result in varying degrees of AV
block. The AV block is usually preceded by intraven-
tricular conduction defect, more commonly RBBB
with or without fascicular block. The AV block is usu-
ally infranodal, at the level of the bundle of His or at
the level of the bundle branches or fascicles. These pa-
tients usually have extensive myocardial damage and
significantly higher mortality than those without AV
block. Implantation of permanent pacemakers in these
patients may prevent bradycardia, but may not alter the
overall prognosis since there is extensive myocardial
damage, which can result in malignant ventricular ar-
rhythmias (Figs. 23.49 and 23.50).
Figures 23.49A,B and 23.50A,B are from the same pa-
tient. There is acute anterior MI complicated by RBBB.
The patient went on to develop complete AV dissocia-
tion (Fig. 23.50A) and subsequently sustained VT (Fig.
23.50B). Patients with acute anterior MI complicated
by intraventricular conduction defect usually have ex-
tensive myocardial damage and are prone to develop
VT/VF. The patient received a permanent pacemaker
and an automatic defibrillator.

RBBB with Acute Inferior MI

ST and T wave are concordant

ST and T wave are concordant

Figure 23.47: Right Bundle Branch Block (RBBB) with ST Elevation Myocardial
Infarction (MI). When RBBB with ST elevation MI is present, the ST segments and T waves
become concordant. Thus, the ST segments (and T waves) are elevated in leads III, aVF, and in
V1 because the QRS complex ends with an R wave and the ST segments are depressed in
leads I, aVL, and V2 because the QRS complex ends with an S wave.
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356 Chapter 23

Figure 23.48: (A) Acute A

Anteroseptal Myocardial
Infarction (MI). ST elevation is
present in V15 consistent with occlu-
sion of the left anterior descending
artery proximal to the first septal per-
forator.The anterior MI was
subsequently complicated by RBBB
as shown by the electrocardiogram
(ECG) in B. (B) Acute MI with RBBB
and Left Anterior Fascicular Block.
This ECG was obtained 14 hours later
from the same patient in (A). The
QRS complexes are wider and a qR
pattern has developed in V1 to V4.
There is also left axis deviation.These B
changes are consistent with acute
anterior MI, RBBB, and left anterior
fascicular block. Note that the diag-
nosis of acute ST elevation MI is pos-
sible even in the presence of RBBB.

Figure 23.49: Right Bundle Branch A: Baseline ECG Prior to MI

Block (RBBB) and Acute Myocardial
Infarction (MI). Electrocardiogram
(ECG) A and B are from the same patient.
(A) Baseline ECG showing left anterior
fascicular block. (B) ECG taken a few
weeks later showing acute anteroseptal
MI complicated by RBBB. The diagnosis of
acute MI is based on the presence of
pathologic Q waves in V1 to V5 and
concordant ST elevation in V1 to V3.There
is also first-degree atrioventricular block
and left anterior fascicular block, which in B: Acute MI + RBBB + LAFB + 10 AV Block
the presence of RBBB may suggest trifas-
cicular block.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 357

A: Complete AV Dissociation Figure 23.50: Acute Myocardial Infarc-

tion and Atrioventricular (AV) Block.
Electrocardiograms A and B are from the same
patient as Figure 23.49. (A) Complete AV disso-
ciation (the P waves are marked by the
arrows). (B) Ventricular tachycardia occurring 5
days later. The patient was successfully resus-
citated and was discharged with a permanent
pacemaker and automatic implantable defib-
rillator.

B. Ventricular Tachycardia

MI in patients with LBBB can be recognized by the fol-

Acute MI and LBBB
LBBB: When LBBB complicates acute MI, the ECG
changes of ST elevation MI may not be recognized be-
cause it is concealed by the conduction abnormality.
This makes diagnosis of acute MI extremely difficult
using the ECG. Among 26,003 patients studied in
GUSTO-1, 131 patients (0.5%) developed LBBB. Acute
lowing ECG findings (Figs. 23.5123.55):
Concordant ST segment: In uncomplicated LBBB
(LBBB without MI), the ST segments are normally
discordant (Fig. 23.51A,B). Thus, the ST segments
are depressed in leads with tall R waves and are ele-
vated in leads with deep S waves. When LBBB is
complicated by acute MI, the ST segments become
concordant (same direction as the QRS complexes)

Figure 23.51: Acute Myocardial

A: V1, V2 , V3 V5, V6, II, III, aVF
B: Infarction (MI) and Left Bundle
Abnormally Branch Block (LBBB). When there
discordant ST
Discordant Segment 5 mm is complete LBBB, the presence of
ST Segment Concordant ST
Concordant ST concordant ST segment deviation 1
Segment 1 mm
Segment 1 mm Discordant mm (A, B) and discordant ST
ST Segment
5 mm elevation 5 mm (A) are consistent
1 mm with acute MI when accompanied by
1 mm symptoms of acute ischemia.

LBBB +
LBBB No MI LBBB + Acute MI LBBB no MI Acute MI
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358 Chapter 23

Figure 23.52: Acute Anterosep- A. Initial ECG:

tal Myocardial Infarction (MI).
The initial electrocardiogram (ECG)
(A) shows acute anteroseptal MI. ECG
(B) taken a few hours later show left
bundle branch block with
concordant ST elevation 1 mm in
lead aVL (arrow).

B. Same Patient as ECG A showing LBBB:

and measure 1 mm. Thus, ST segment depression
1 mm in leads with deep S waves (V1, V2, or V3;
Fig. 23.51A) or ST elevation 1 mm in leads with
tall R waves (V5, V6, and often in II, III, and aVF; Fig.
23.51B) are consistent with acute ST elevation MI.
Discordant ST segment: Acute MI can also be di-
agnosed if the ST segments are abnormally discor-
dant (opposite direction to the QRS complexes) and
measure 5 mm. Thus, ST elevation 5 mm in any
lead with deep S waves such as V1 to V3 is consistent
with acute MI when accompanied by symptoms of
acute ischemia (Fig. 23.51A).
The two ECGs (Figs. 23.54 and 23.55) show discordant
ST segments. In Figure 23.54, discordant ST segment
elevation of more than 5 mm is present in V2 and V3.
These ECG changes are associated with symptoms of
acute ischemia. In Figure 23.55, there is concordant ST
segment depression in V4, which is accepted as a crite-
rion for acute MI. In addition, there is also discordant
ST segment depression of 5 mm in V5. Presently, dis-
cordant ST depression 5 mm is not included in the
literature as a criterion for acute MI in the presence of
LBBB.
Common Mistakes in ST Elevation MI
Other causes of ST elevation: There are several other
causes of ST elevation other than acute MI. These entities

Figure 23.53: Acute Myocardial

Infarction (MI) and Left Bundle
Branch Block (LBBB). LBBB is
present with wide QRS complexes
measuring 0.12 seconds.
Concordant ST segment elevation
1 mm is present in leads with tall R
waves including V5, V6, and leads II, III,
and aVF (arrows) consistent with
acute ST elevation MI.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
should be recognized especially when thrombolytic
agents are being considered as therapy for the acute MI.
Normal elevation of the ST segment at the transi-
tion zone
Early repolarization
LBBB
Left ventricular hypertrophy (LVH)
Acute pericarditis
Left ventricular aneurysm
Electrolyte abnormalities: hyperkalemia and hyper-
calcemia
Wolff-Parkinson-White (WPW) syndrome
Osborn wave of hypothermia
Brugada ECG
Others: Pacemaker rhythm, ectopic ventricular
complexes, Takotsubo cardiomyopathy, tumors or
trauma involving the ventricles.
ST elevation at the transition zone: Elevation of the
ST segment is common in normal individuals at the
precordial transition zones V2, V3, or V4. The transition
zone is at the mid-precordial leads, where the R wave
becomes equal to the S wave as the precordial elec-
trodes move up from V1 to V6. The ST segments in
25 % in V6. This ratio is helpful when peri-
these transition leads have upsloping configuration
and are usually not isoelectric. The elevation of the ST
359
Figure 23.54: Acute Myocardial
Infarction (MI) and Left Bundle
Branch Block (LBBB). LBBB is
present with discordant ST segment el-
evation 5 mm in V2 and in V3 (arrows),
which in the presence of symptoms
chest pain indicate acute MI.
segment is a normal and expected finding and should
not be considered a variant of normal (Fig. 23.56).
Early Repolarization: J point elevation with ST eleva-
tion from early repolarization is common in normal
individuals. The ST elevation is usually seen in the pre-
cordial leads and can be mistaken for transmural my-
ocardial injury. The following are the characteristic fea-
tures of early repolarization:
ST elevation is commonly seen in leads V2 to V6 and
also in leads II, III, and aVF. The ST elevation is con-
cave upward (Fig. 23.57).
Early repolarization is not accompanied by recipro-
cal depression of the ST segment.
A prominent notch is usually inscribed at the termi-
nal portion of the QRS complex in leads with ST
elevation (Fig. 23.57).
The ST elevation usually becomes isoelectric or less
pronounced during tachycardia and becomes more
accentuated during bradycardia (Figs. 23.58 and
23.59).
The T waves in V6 are usually tall when compared with
the height of the ST segment. Thus, the ratio between
the height of ST segment and that of the T wave is
usually
carditis is being considered. Elevation of the ST seg-
ments in pericarditis is usually prominent. Thus,
Figure 23.55: Discordant
Pattern. This patient ruled in for
acute myocardial infarction (MI) with
markedly elevated troponins. The
electrocardiogram shows left bundle
branch block (LBBB) with concordant
ST segment depression 1 mm in V4.
There is also discordant ST segment
depression 5 mm in V5 (arrows).
Discordant ST depression is
presently not included as a criterion
for acute MI when there is LBBB.
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360 Chapter 23

Figure 23.56: Normal ST Elevation at the Transition Zone. Elevation of the ST seg-
ment is common in normal individuals at the transition zone which is usually in V2, V3, or V4
(arrows).This is a normal finding often described as high take-off of the ST segment. Very
often, the T waves are also peaked and taller than the R wave at the transition zone. This is
also a normal finding.

Notch at the J point

Concave ST elevation

ST-T ratio in V6 <25%

6 mm

1 mm

Figure 23.57: Early Repolarization. ST segment elevation is noted in V3 to V6 (arrows), which can be
mistaken for acute myocardial injury. There is no reciprocal ST depression in any lead and a prominent notch is
present at the end of the R wave in V4. Note that the height of the ST segment in V6 measures 1.0 mm and the
height of the T wave measures 6 mm (ST elevation/T wave ratio 25%). A ratio
25% suggests early repolariza-
tion. If pericarditis is being considered, the ratio is 25% because the height of the T waves is generally lower in
pericarditis.

HR 92 BPM HR 70 BPM HR 44 BPM

Figure 23.58: Early Repolarization during Holter Monitoring. Three rhythm

strips with different heart rates are shown above in the same patient undergoing Holter
monitoring. Note that there is more pronounced ST segment elevation because of early re-
polarization when the heart rate is slower than when the heart rate is faster. Arrows point to
the ST segment elevation. HR, heart rate.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
A: Baseline ECG (HR 84 BPM) B: Maximal Exercise (HR 146 BPM)
when the ratio between the height of the ST segment
compared with that of the height of the T wave is
25% in V6, pericarditis is the more likely diagnosis.
In early repolarization, the ST segment elevation is
more prominent when the heart rate is slower as shown
in Figures 23.58 and 23.59.
Hyperkalemia: Hyperkalemia can cause elevation of
the ST segment in the ECG (see Chapter 25, Elec-
trolyte Abnormalities). The ST segment elevation can
be mistaken for acute ST elevation MI (Fig. 23.60).
When ST segment elevation of this magnitude occur
during hyperkalemia, the serum potassium level is
usually 8 mEq/L.
LBBB: In LBBB, the ST segments and T waves are nor-
mally discordant with the QRS complex. Thus, ST seg-
ment elevation and upright T waves are recorded in
361
Figure 23.59: Early
Repolarization Before and Dur-
ing Maximal Exercise. (A) A 12-
lead baseline electrocardiogram from
a 56-year-old male.The baseline heart
rate was 84 beats per minute. ST seg-
ments were elevated in II, III, aVF, and
V2 to V6. (B) The same patient during
maximal exercise. Heart rate was 146
beats per minute. The ST segments
have become isoelectric.
leads with deep S waves such as V1 to V3 and ST de-
pression with inverted T waves recorded in leads with
tall R waves such as V5 or V6 (Fig. 23.61).
LVH: When LVH is present, the ST segment and T wave
become discordant. ST depression and T wave inversion
are recorded in leads with tall R waves; ST elevation
and upright T waves are recorded in leads with deep S
waves. Thus, ST elevation is usually present in V1 to V3
because deep S waves are normally expected in these
leads when there is LVH (Fig. 23.62).
Brugada ECG: The Brugada ECG is an electrocardio-
graphic abnormality confined to leads V1 and V3. There
is RBBB configuration with rSR pattern in V1 or V2.
The J point and ST segment are elevated measuring 1
mm, with a coved or upward convexity terminating
into an inverted T wave (Fig. 23.63).
Figure 23.60: ST Elevation from
Hyperkalemia. The electrocardio-
gram can be mistaken for acute my-
ocardial infarction (MI) resulting from
the marked ST-T changes resembling
acute ST elevation MI. Note the pres-
ence of peaked T waves in virtually
all leads.
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362 Chapter 23
Figure 23.61: ST Elevation from
Left Bundle Branch Block
(LBBB). In LBBB, ST elevation
(arrows) is usually seen in leads with
deep S waves such as V1 to V3.
Brugada ECG: The Brugada ECG associated with
symptoms of VT/VF is called the Brugada syndrome.
The Brugada syndrome is not associated with struc-
tural heart disease or prolonged QTc, but is a genetic
disease that can cause sudden cardiac death. The ab-
normality is the result of a defect in the sodium chan-
nel of myocytes in the epicardium of the right ventricle
and is inherited as an autosomal dominant pattern.
The ST elevation in V1 and in V2 may be saddle shaped
or triangular instead of coved in configuration and the
ECG abnormality may wax and wane (Fig. 23.64A,B).
The significance as well as prognosis of asymptomatic
patients with the Brugada ECG is unknown since not
all patients with the Brugada ECG will develop ventric-
ular arrhythmias or syncope (see Chapter 21, Ventricu-
lar Arrhythmias).
Hypothermia: Hypothermia is characterized by J
point elevation. The J point marks the end of the QRS
complex and beginning of the ST segment. A markedly
elevated J point is also known as J wave or Osborn
wave. The J wave is shaped like a letter h. The magni-
tude of the J point elevation follows the severity of the
hypothermia (Fig. 23.65A) and disappears when the
temperature is restored to normal (Fig. 23.65B).
Acute pericarditis: Acute pericarditis or inflamma-
tion of the pericardium is associated with diffuse ST
segment elevation (Fig. 23.66A). The ST elevation usu-
Figure 23.62: ST Elevation
from Left Ventricular Hypertro-
phy (LVH). Elevation of the ST seg-
ment in LVH is frequently seen in V2
and V3, as shown by the arrows.
ally involves almost all leads. Reciprocal ST depression
is confined to leads V1 and aVR. Depression of the P-R
segment is often present. Unlike ST elevation MI, the
ST elevation in acute pericarditis does not evolve into q
waves. The ST elevation usually persists for a week fol-
lowed by T wave inversion. It may take another week or
more before the inverted T waves revert to normal.
Left ventricular aneurysm: ST segment elevation
that does not resolve after acute transmural MI usually
suggests the presence of a left ventricular aneurysm.
The ST segment elevation is present in leads with Q
waves. The T waves are usually inverted. Almost all
aneurysms are located at the anteroapical wall of the
LV and, much less commonly, the base of the inferior
wall. The elevation of the ST segment is usually perma-
nent (Fig. 23.67). In this era of reperfusion therapy, the
presence of a left ventricular aneurysm should be
suspected in patients with ST elevation MI when
pathologic Q waves occur and the ST elevation does
not resolved within a few days.
Pacemaker-induced ventricular complexes: ST el-
evation is also seen in pacemaker captured ventricular
complexes (Fig. 23.68) and ectopic ventricular rhythms.
The ST elevation is secondary to the abnormal activa-
tion of the ventricles.
Takotsubo cardiomyopathy: Takotsubo cardiomy-
opathy (CMP), also called left ventricular apical
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
ballooning syndrome, is increasingly becoming more
recognized as a clinical entity characterized by sub-
sternal chest pain accompanied by ECG changes iden-
tical to the ECG of acute coronary syndrome. These
includes ST elevation, ST depression, T wave inver-
sion and development of pathologic Q waves. The
most common presentation is ST elevation involving
the anterior precordial leads. These ECG changes are
accompanied by mild troponin elevation. Unlike
acute coronary syndrome, which results from throm-
botic occlusion of the coronary artery, Takotsubo
CMP is associated with normal coronary arteries.
A.
B.
363
Figure 23.63: Brugada Electro-
cardiogram (ECG) with Convex
ST Segment. The Brugada ECG
has a right bundle branch block pat-
tern in V1 to V3 with J point elevation,
coved ST segment, and inverted T
waves (arrows). Courtesy of Athol
Morgan, MD.
There is ballooning of the anteroapical left ventricular
wall and compensatory hyperkinesis of the basal seg-
ments. This angiographic appearance resemble an oc-
topus trap (takotsubo) and is usually reversible. Al-
though originally described in Japan it is increasingly
recognized in Europe and the United States, mostly in
post-menopausal women who have experienced
physical or emotional distress. The cause of the CMP
is uncertain although it is probably related to exces-
sive sympathetic stimulation, microcirculatory dys-
function, or myocardial stunning resulting from se-
vere multivessel coronary spasm.
Figure 23.64: Brugada Electro-
cardiogram (ECG) with
Concave ST Segment. The ST
elevation in V1 and V2 (A) is concave
(saddle back), which is another type
of ST elevation in the Brugada ECG.
(B) The saddle back pattern has dis-
appeared.
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Figure 23.65: Hypothermia. A. a

The initial electrocardiogram (ECG)
shows Osborn waves (arrows) repre-
senting elevation of the J point due
to hypothermia. There is also sinus
bradycardia with a rate of 50 beats
per minute. ECG B was taken 4 hours
after the initial ECG. The Osborn
waves have disappeared.

B. 4 hours later

Figure 23.66: Acute Pericarditis. A. On admission

The initial electrocardiogram (ECG)
(A) on admission shows diffuse ST el-
evation in almost all leads consistent
with acute pericarditis. The ST-T ratio
in V6 is 25% (arrow). ECG (B) was
obtained 4 to 5 weeks later showing
ST depression, T inversion but no
pathologic Q waves.

B. 5 weeks later

364
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction 365

Figure 23.67: Left Ventricular Aneurysm. ST segment elevation persists more than 5
years after acute ST elevation myocardial infarction from left ventricular aneurysm. Note that
the ST segment elevation is confined to leads with pathologic Q waves V1 to V4 (arrows).The
ST segments have an upward convexity and the T waves are inverted. Echocardiogram and
nuclear perfusion scans confirmed the presence of an anteroapical left ventricular aneurysm.

a routine ECG and may be the only marker that a pre-

Q Waves
Q waves: Q waves associated with acute ST elevation
MI generally indicate transmural myocardial necrosis,
which is a more advanced stage of myocardial involve-
ment. Q waves, which mark the area of transmural
necrosis, signify permanent myocardial damage. Al-
though Q waves are the usual sequelae of ST elevation
MI, not all patients with ST elevation MI will develop
Q waves. Additionally, some patients with non-ST ele-
vation MI may develop Q waves. Thus, ST elevation MI
is a more concise terminology instead of Q-wave MI.
The development of Q waves during ST elevation MI
may take a few hours to several days, depending on
collateral flow. When collaterals are absent or are in-
adequate, Q waves may develop very early, within a
few hours after symptom onset and may be present
when the initial ECG is recorded (Fig. 23.69). Similar
to ST elevation, pathologic Q wave serves as a useful
marker in identifying the infarct related coronary ar-
tery, even after the ST-T abnormalities have resolved.
Pathologic Q waves may be recorded unexpectedly in
vious MI had occurred.
The presence of Q waves during ST elevation MI is not
a contraindication to thrombolytic therapy. Progres-
sion of ST elevation MI to a Q wave MI may be pre-
vented if reperfusion is timely and successful.
Normal Q waves: Q waves may be normal or abnor-
mal. Normal Q waves represent activation of the ven-
tricular septum in a left to right direction (see Chap-
ter 6. Depolarization and Repolarization). These Q
waves are often called septal Q waves. Septal Q waves
are normally recorded in leads located at the left side
of the ventricular septum including V5, V6, and leads
I and aVL. The size of the normal Q wave is variable
and depends on the thickness of the ventricular sep-
tum. In normal individuals, the Q waves are usually
narrow measuring 0.03 seconds in duration and
are 25% of the height of the R wave. Q waves in
lead III do not represent septal Q waves. Thus, the Q
waves in lead III may be wide and deep but are not
necessarily pathologic even when it exceeds 0.03 sec-
onds in duration.
Abnormal Q waves: The differential diagnosis of
abnormal Q waves is limited to a few conditions.

Figure 23.68: ST Elevation from Pacemaker-Induced Ventricular Rhythm. Lead

II rhythm strip showing ST elevation during pacemaker captured ventricular complexes (ar-
rows) but not in normally conducted complexes. The ST segment elevation is secondary to
abnormal activation of the ventricles.
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366 Chapter 23

Figure 23.69: Acute Anteroseptal Myocardial Infarction (MI). Initial electrocardio-

gram of a patient with chest pain showing deep Q waves in V1 to V3 with marked ST
elevation across the precordium consistent with acute extensive anterior MI. Note the early
appearance of QS complexes in V1 to V3, suggesting the presence of transmural myocardial
necrosis involving the anteroseptal wall. Coronary angiography showed complete occlusion
of the left anterior descending coronary artery after the first diagonal branch.

These include transmural MI, idiopathic hyper-
trophic subaortic cardiomyopathy, LVH, abnormal
activation of the ventricles from WPW syndrome,
LBBB and fascicular blocks, myocardial scarring
from cardiomyopathy, infiltrative disease involving
the myocardium, or when the rhythm is ectopic or
pacemaker induced.
Pathologic Q Waves
Pathologic Q waves from transmural myocardial
necrosis: Pathologic Q waves from transmural
necrosis are easy to identify during the acute episode
when they are accompanied by ST elevation and T-
wave abnormalities. However, when the MI is remote
and the ST-T abnormalities have resolved, Q waves
from transmural necrosis may be difficult to differ-
entiate from normal septal Q waves. The following
are the features of pathologic Q waves due to trans-
mural myocardial necrosis or clinically established
MI according to a joint European Society of Cardiol-
ogy and American College of Cardiology committee
proposal.
In leads I, II, aVL, aVF, V4, V5, or V6: a pathologic
Q wave should measure 0.03 seconds in dura-
tion. The abnormal Q wave must be present in
any two contiguous leads and should be 1 mm
deep.
In V1, V2, and V3: any Q wave is pathologic regard-
less of size or duration.
QRS confounders such as LBBB, LVH, and WPW
syndrome should not be present.
Similar to ST segment elevation, pathologic Q waves
are specific in localizing the area of the transmural MI.
Some Q waves, however, are not permanent. Contrac-
tion of the scar tissue may occur during the healing
process and may cause the Q waves to become nar-
rower and may even disappear.
Inferior MI: The diagnosis of inferior MI is based on
the following:
Q in II and aVF are 0.03 seconds in duration and
are 1 mm deep.
Q in Lead III 0.04 seconds in duration or the Q
waves have an amplitude of 5 mm or 25% of the
height of the R wave plus a Q wave in aVF that is
0.03 seconds in duration and 1 mm deep.
A QS complex in lead III alone, no matter how deep or
wide, is not enough to make a diagnosis of inferior MI.
Anterior MI: The diagnosis of anterior MI is based on
the following:
Q waves in V1: Although the 2000 European Soci-
ety of Cardiology (ESC)/ACC proposal on the rede-
finition of MI mentions that any size Q wave is ab-
normal in V1, V2, or V3, the more recent 2007 ESC/
American College of Cardiology Foundation
(ACCF)/AHA/World Health Federation (WHF)
consensus document on the universal definition of
MI considers a QS complex in V1 as a normal find-
ing. Q waves in V1 and in V2 have also been shown to
be normal in some patients with chronic pulmonary
disease because the diaphragm is displaced down-
ward. It may also be a normal finding when the elec-
trodes are inadvertently misplaced at a higher loca-
tion at the second instead of the fourth intercostal
space.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
Q waves in V1 To V3: When Q waves are present in
V1 to V3, they are pathologic regardless of size or du-
ration since normal septal q waves are not normally
recorded in all three leads. Other causes of q waves
such as LVH, fascicular block, LBBB, and WPW
ECG should be absent.
Poor R wave progression: The size of the R wave
does not increase from V1 to V4. This may be due to
anterior MI, although this finding is less specific
for anterior MI because this may be caused by sev-
eral other conditions that can cause clockwise ro-
tation (see Chapter 4, The Electrical Axis and Car-
diac Rotation).
Posterior or inferobasal MI: Posterior MI will
show tall R waves in V1 or V2. The tall R waves are re-
ciprocal changes due to the presence of deep Q
waves over the posterior wall. If special leads V7 to V9
are recorded, QS complexes will be present. Other
causes of tall R waves in V1 and V2 are further dis-
cussed in Chapter 4, The Electrical Axis and Cardiac
Rotation.
Lateral MI: Q waves 0.03 seconds in I and aVL or in
V5 and V6 or in all four leads are pathologic and consis-
tent with lateral MI.
367
Figure 23.70: Pathologic Q
waves due to Idiopathic Hyper-
trophic Subaortic Stenosis
(IHSS). Pathologic Q waves are
noted in V26, as well as in leads I and
aVL from idiopathic hypertrophic
cardiomyopathy. The Q waves in
IHSS represent normal activation of
an unusually thick septum, which is
often two to three times thicker than
a normal septum.These Q waves can
be mistaken for anterolateral
myocardial infarction.
Other Causes of Pathologic Q Waves
Pathologic Q waves resulting from idiopathic hy-
pertrophic subaortic stenosis (IHSS): When there is
excessive thickening of the ventricular septum such as
IHSS, the septal Q waves become exaggerated and can
be mistaken for Q waves of MI (Fig. 23.70).
Pathologic Q waves from preexcitation: The pres-
ence of preexcitation (WPW ECG) can also cause abnor-
mal Q waves that can be mistaken for MI (Fig. 23.71).
Pathologic Q waves from LBBB: Activation of the LV is
abnormal when there is LBBB. In LBBB, deep QS com-
plexes in V1,2,3 and often in leads II, III, and aVF are not
necessarily pathologic (Fig. 23.72). However, any size Q
wave in V5 and V6 is pathologic when there is LBBB be-
cause the ventricular septum is activated from right to left
and Q waves should not be present in these leads. In
LBBB, Q waves in V5,6 indicate a septal infarct (Fig. 23.73).
Pathologic Q waves resulting from ectopic ven-
tricular rhythms: Accelerated idioventricular rhythm,
ventricular tachycardia, or ventricular pacemaker
rhythm may cause Q waves from abnormal activation
of the ventricles.
Figure 23.71: Pathologic Q
waves from Preexcitation. Deep
Q waves are seen in V1, V2, V3, and
leads III and aVF from preexcitation
(Wolff-Parkinson-White
electrocardiogram).These Q waves
represent delta waves directed pos-
teriorly and inferiorly can be
mistaken for anteroseptal or inferior
myocardial infarction.
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368 Chapter 23

Figure 23.72: Q Waves in Left

Bundle Branch Block (LBBB).
QS complexes are present in leads III,
aVF, and V1 to V3 (arrows), which can
be mistaken for myocardial
infarction. These QS complexes are
not pathologic and do not indicate a
Q wave infarct when LBBB is present.

be divided into those with and those without ST elevation.

Acute Coronary Syndrome
ECG Findings ECG Findings of ST Elevation
Myocardial Infarciton
The ECG of acute coronary syndrome can be divided into
two types:
ST segment elevation
Non-ST segment elevation
n ST segment depression
n T-wave inversion
n Other less specific ST and T wave abnormalities
ECG changes of ST elevation myocardial infarction:
ST segment elevation of 1 mm in two or more adjacent
leads
New or presumed new-onset LBBB
Development of pathologic Q waves
ST Elevation versus Non-ST Elevation
Acute coronary syndrome is usually the result of rupture of
an atherosclerotic plaque resulting in obstruction of the ves-
sel lumen by a thrombus. Depending on the severity of coro-
nary obstruction, thrombotic occlusion of the vessel lumen
may cause varying degrees of myocardial ischemia, which can
These two ECG abnormalities have distinctive pathologies
and have different prognostic and therapeutic significance.
ST segment elevation: Acute coronary syndrome with
ST elevation in the ECG indicates that one of the three
epicardial coronary arteries is totally occluded with TIMI
0 flow (Thrombolysis in Myocardial Infarction grade flow
indicating no antegrade flow beyond the point of occlu-
sion). Thrombotic occlusion of the vessel lumen with ST
segment elevation almost always results in cellular necro-
sis with elevation of the cardiac troponins in the circula-
tion. If myocardial perfusion is not restored in a timely
manner, changes in the QRS complex with development
of Q waves or decreased amplitude of the R waves will oc-
cur. Acute coronary syndrome from coronary vasospasm
can also cause ST elevation although coronary vasospasm
is usually transient and responds to coronary vasodilators
such as nitroglycerin.
Non-ST segment elevation: When the vessel lumen is
partially occluded by a thrombus, myocardial ischemia
may or may not occur depending on the severity of coro-
nary artery obstruction, presence of collateral flow and
myocardial demand for oxygen. Even if the vessel lumen
is partially occluded if myocardial oxygen demand does
not exceed its blood supply, myocardial ischemia may not
develop. If myocardial ischemia occurs, it may or may not
result in myocardial necrosis.

Figure 23.73: Left Bundle

Branch Block (LBBB) and Septal
Q Waves. When there is LBBB, sep-
tal Q waves should not be present in
V5 or V6 or in leads I or aVL. When Q
waves are present in these leads (ar-
rows), no matter how small or micro-
scopic, these Q waves are pathologic
and indicate a septal myocardial in-
farction.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
n Non-ST elevation MI: Partial occlusion of the vessel
lumen accompanied by cellular necrosis indicates
non-ST elevation MI. The most important marker of
cellular necrosis is increased cardiac troponins in the
circulation. The diagnosis of non-ST elevation MI is
not established unless these cardiac markers are ele-
vated. The ECG will show ST segment depression, T
wave inversion, or less-specific ST and T wave abnor-
malities. Occasionally, the ECG may not show any sig-
nificant abnormalities.
n Unstable angina: In unstable angina, the ECG changes
are identical to that of non-ST elevation MI, although
the cardiac troponins are not elevated in the circulation.
Acute MI: With the advent of troponins as a marker of my-
ocardial necrosis, acute MI was redefined in 2000 by a con-
sensus document of the ESC/ACC and again in 2007 by the
ESC/ACCF/AHA/WHF, as myocardial necrosis in a clinical
setting consistent with myocardial ischemia.
Myocardial necrosis: Myocardial necrosis is based on
the rise and/or fall of cardiac troponins.
Myocardial ischemia: Evidence of myocardial ischemia
is based on any of the following:
n Clinical symptoms of ischemia
n ECG changes indicative of new ischemia, which in-
cludes any of the following:
n New ST-T changes
n New LBBB
n Development of pathologic Q waves
n Imaging abnormalities
n New loss of viable myocardium
n New regional wall motion abnormality
Thus, increased in cardiac troponins in the circulation is the
most important marker of myocardial necrosis. The diagno-
sis of acute MI is not possible unless the troponins are
elevated. If sudden cardiac death occur before blood samples
for troponins could be obtained or before troponins become
elevated, acute MI is diagnosed by the associated symptoms
and ECG changes of myocardial ischemia.
Clinical Implications
ST segment elevation from acute coronary syndrome indi-
cates complete obstruction of the vessel lumen. Therapy re-
quires that coronary blood flow be restored immediately.
T-wave inversion and ST segment depression indicate less se-
vere form of myocardial ischemia from a combination of di-
minished coronary blood flow and increased myocardial
oxygen demand. Immediate therapy for T-wave inversion
and ST segment depression is directed toward stabilizing the
thrombus and lowering myocardial demand for oxygen.
ST segment elevation: Thrombotic occlusion of the vessel
Identifying the Infarct-Related Artery
lumen with persistent elevation of the ST segment is always as-
sociated with troponin elevation. Unless adequate collaterals
are present or unless the occluded coronary artery is immedi-
369
ately reperfused, virtually all myocardial cells supplied by the
totally occluded artery become irreversibly damaged within 6
hours after symptom onset. No significant pathologic abnor-
malities in the myocardium may be detected microscopically,
if the patient dies suddenly within this period. The ECG, how-
ever, is very useful in identifying the presence of acute trans-
mural ischemia and in timing the various stages of the infarct.
Hyperacute T waves: Hyperacute T waves are usually
the earliest ECG abnormality to occur in ST elevation MI.
The presence of peaked and tall T waves overlying the
area of ischemia often occur very early during the initial
onset of symptoms and is often helpful in timing the on-
set of an acute ischemic process. The hyperacute T waves
may be due to local hyperkalemia or presence of an elec-
trical gradient between normal and injured myocardial
cells during electrical systole.
ST Elevation: When ST elevation is present, it is usually
the most striking abnormality in the ECG during the acute
phase of myocardial ischemia. The magnitude of ST eleva-
tion is measured at the J point. ST elevation is usually con-
fined to leads geographically representing the territory
supplied by the occluded artery. Thus, the presence of ST
elevation is helpful in identifying the infarct related artery.
The greater the number of leads with ST elevation and the
more pronounced the ST elevation, the more severe the
myocardial ischemia and the more extensive the myocar-
dial damage. Myocardial ischemia, which is reversible, may
be severe and relentless and transition to necrosis, which is
irreversible, may be completed within 6 to 24 hours after
onset of symptoms. This transition is highly variable and
often unpredictable because of collateral flow and remod-
eling within the thrombus. For example, if the thrombus
undergoes spontaneous lysis and rethrombosis, the symp-
toms and ECG findings may wax and wane and the above
sequence of evolution may take several days or even weeks
before the infarct is finally completed.
Q waves: ST elevation MI generally results in the devel-
opment of pathologic Q waves or diminution in the size
of the R waves. Q waves are pathologic when they meas-
ure 0.03 seconds in duration and are at least 1 mm
deep in leads I, II, AVF, aVL, and V4 to V6. Any size Q wave
is pathologic when present in V2 and also in V3. The pres-
ence of pathologic q waves indicates transmural necrosis,
which is usually permanent. Although ST elevation MI is
synonymous with Q wave MI, Q waves may not always
occur especially if the occluded coronary artery is revas-
cularized in a timely fashion. Additionally, approximately
25% of patients with non-ST elevation MI may develop Q
waves; thus, non-ST elevation MI rather than Q wave MI
is the preferred terminology.
ST segment elevation or pathologic Q waves in the ECG is
useful in identifying the location of the infarct-related artery.
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370 Chapter 23
When ST elevation or Q waves are localized in the ante-
rior precordial leads V1 to V4 (or to V6), acute anterior MI
is present. This identifies the LAD artery as the culprit
vessel. The ESC/ACC task force on the redefinition of
acute MI requires that ST elevation in V1 to V3 should be
present in at least two leads and should measure 2 mm
in contrast to other leads which requires only 1 mm of ST
elevation.
When ST elevation or pathologic Q waves occur in leads
II, III, and aVF, acute inferior MI from occlusion of the
posterior descending coronary artery is present. The RCA
is the culprit vessel in 85% to 90% of patients with acute
inferior MI and the LCx coronary artery in the remaining
10% to 15%. Inferior MI may also occur when there is an-
terior MI because the LAD may circle the apex of the LV
and extend inferoapically. This is not a true inferior MI
because the posterior descending coronary artery is not
involved. This is merely an extension of the anterior MI.
When ST elevation or pathologic Q waves are confined to
leads I and aVL or leads V5 and V6, acute lateral MI is
present and identifies the LCx coronary artery as the cul-
prit vessel. This is often associated with ST depression in
V2 and in V3.
The posterolateral wall of the LV is not represented in the
standard 12-lead ECG. Acute posterolateral MI with ST
segment elevation in V7, V8, and V9 may not be recognized
because these leads are not routinely recorded. It is usu-
ally suspected when there is ST elevation in V6 and ST de-
pression in V2 and V3. Tall R waves may also be present in
V1 and V2, which are reciprocal changes due to the pres-
ence of deep Q waves posterolaterally. This usually identi-
fies the LCx as the culprit lesion, although, occasionally, it
may be due to a dominant RCA.
LAD Coronary Artery
Area supplied: The LAD is a large artery that supplies the
whole anterior wall of the LV. It is the main blood supply to
the intraventricular conduction system including the bundle
of His, bundle branches, and distal fascicular system.
Anatomy: The LAD courses through the anterior interven-
tricular groove and supplies the ventricular septum and an-
terior wall of the LV.
The length of the LAD can be short (terminates before the
apex), medium (terminates at the apex), or large (wraps
around the apex and continues to the inferior wall of the LV).
The first branch of the LAD is the first diagonal (D1),
which courses laterally between the LAD and left circum-
flex coronary artery. Usually one to three diagonal
branches are given off by the LAD. D1 is often the largest
diagonal branch and supplies the base of the anterolateral
wall of the LV.
The second branch is the first septal branch (S1). S1 may
be the first instead of the second branch. About three to
five septal branches arise at right angles from the LAD
and directly insert perpendicularly into the myocardium
and supply the anterior two thirds of the ventricular sep-
tum. S1 supplies the basal anteroseptal region of the LV
and is the main blood supply of the distal His bundle and
proximal left and right bundle branches.
Occlusion of the proximal LAD: The following is a sum-
mary of the ECG findings when complete occlusion involves
the proximal LAD:
Occlusion of the LAD before the first branch (D1 or S1):
n ST elevation in V1 to V4 (anteroseptal) and leads I and
aVL (basal lateral or high lateral wall). Because the
first septal branch or S1 supplies the base of the ven-
tricular septum, ST elevation will occur in V1.
n ST elevation in aVL. Because the first diagonal branch
or D1 supplies the base of the lateral wall, ST elevation
will occur in aVL.
n Reciprocal ST depression is present in III and aVF
(from ST elevation in aVL, which is diametrically op-
posite lead III)
n If ST elevation is confined to V1 to V3, reciprocal ST
depression may be present in V5 or V6.
n Complete RBBB may occur.
n If the LAD is large and extends to the left ventricular
apex and contiguous inferior wall, ST elevation may
occur in leads II, III, and aVF (acute inferior MI), in
addition to the ST elevation in the precordial leads.
n ST elevation may be present in aVR.
Occlusion of the LAD distal to the first diagonal and
first septal branches:
n Occlusion of the LAD distal to D1 and S1 results in a
less extensive infarct compared with a more proximal
lesion and will cause ST elevation only in V2 to V4.
n ST elevation will not occur in V1 nor lead aVL or lead
I because the first septal and first diagonal branches
are spared. Because ST elevation is not present in
lead aVL, reciprocal ST depression will not occur in
lead III.
Common Complications Associated with Acute Ante-
rior MI:
Tachyarrhythmias: Ventricular fibrillation is the most
common cause of death usually within the first few hours
after symptom onset. Although ventricular tachycardia
and fibrillation can occur in any patient with acute MI,
acute anterior myocardial infarction is more commonly
associated with tachyarrhythmias including sinus tachy-
cardia, ventricular tachycardia, and ventricular fibrilla-
tion in contrast to inferior MI, which is usually associated
with bradyarrhythmias such as sinus bradycardia and
varying degrees of AV block.
Intraventricular conduction defects: Occlusion of the
LAD proximal to the first septal branch can jeopardize the
conduction system and can cause transient or permanent
conduction abnormalities.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
n RBBB with or without fascicular block: This is usually
from the involvement of the first septal branch of the
LAD. Diagnosis of acute MI in the presence or RBBB is
not difficult because activation of the LV is not altered.
n LBBB: LBBB is less frequently seen as a complication
of MI compared with RBBB. Although LAD disease is
commonly expected to cause LBBB, LBBB complicat-
ing acute MI are usually non-anterior in location with
the lesion more commonly associated with the right
rather than left coronary artery as shown in the subset
analysis of patients with acute MI in the GUSTO-1
databases. The diagnosis of acute MI in the presence
of LBBB is difficult because the LV is activated abnor-
mally from the right bundle branch. This was previ-
ously discussed in Chapter 10, Intraventricular
Conduction Defect: Bundle Branch Block.
Complete AV block: When complete AV block occurs in
the setting of acute anterior MI, the AV block is infran-
odal because the LAD supplies most of the distal intra-
ventricular conduction system. The AV block is often pre-
ceded by RBBB with or without fascicular block.
Prognosis remains poor even with temporary or perma-
nent pacing because occlusion of the LAD complicated by
RBBB is usually an extensive MI. Atropine does not re-
verse the AV block because the conduction abnormality is
infranodal, at the His-Purkinje level. The indication for
the implantation of permanent pacemakers in patients
with intraventricular conduction defect and AV block as-
sociated with acute MI is discussed under treatment.
LV dysfunction and pump failure: Acute anterior MI is
associated with a higher incidence of heart failure and
cardiogenic shock. Cardiogenic shock usually occurs
when at least 40% of the left ventricular myocardium is
involved. Heart failure and cardiogenic shock are more
common with acute anterior MI because acute anterior
MI is generally a large infarct.
Late ventricular arrhythmias and sudden death: Pa-
tients with extensive myocardial damage and severe left ven-
tricular dysfunction who survive their MI are at high risk for
ventricular arrhythmias and sudden death. These complica-
tions are more frequently seen in patients with anterior MI.
LCx Artery
Anatomy and area supplied: The LCx coronary artery cir-
cles around the left or lateral AV groove and sends three or
more obtuse marginal branches to the lateral wall of the LV.
Right Coronary Artery
It continues posteriorly as the posterior AV artery sending
three or more posterolateral branches to the LV. In 10% to
15% of patients, the LCx artery continues as the posterior de-
scending coronary artery, which supplies the inferior wall of
the LV. When this occurs, the pattern of coronary distribu-
tion is described as left dominant.
Occlusion of the LCx: The following is a summary of the
ECG changes when the LCx coronary artery is occluded:
371
Acute lateral MI with ST elevation (or pathologic Q
waves) in I and aVL or V5 and V6 with or without ST de-
pression in V1 to V3.
Acute inferior MI with ST elevation or pathologic Q waves
in II, III, and aVF if the LCx artery is the dominant artery.
No significant ECG changes. When acute MI is diagnosed
clinically without significant ECG changes, the culprit
vessel is usually the LCx coronary artery.
Unless there is unusual variation in coronary anatomy,
occlusion of the LCx coronary artery does not result in
right ventricular infarction.
Straight posterior MI or acute posterolateral MI with
prominent q waves and ST elevation in special leads V7,
V8, and V9. Tall R waves may be present in V1 and V2 with
reciprocal ST depression from V1 to V3.
n If the MI involves the basal posterior wall of the LV or
is directly posterior or posterolateral, the ECG will
show reciprocal ST depression in V1 to V3 because
these leads are diametrically opposite the posterior or
posterolateral wall. Unfortunately, ST depression in V1
to V3 can be mistaken for ischemia involving the ante-
rior wall of the LV rather than a transmural posterior
MI. This dilemma can be resolved by recording extra
leads V7, V8, and V9, which overlie the posterolateral
wall of the LV. Leads V7 to V9 will show ST elevation if
an acute transmural posterolateral MI is present but
not when there is anterior wall ischemia and injury.
ST elevation of 0.5 mm is significant because of the
wider distance between these leads in relation to the
heart. ST elevation in V7 to V9 makes the patient a can-
didate for thrombolytic therapy.
n Tall R waves in V1 to V2 may also occur although these
changes usually develop several hours later.
Common Complications Associated with Acute Lateral
or Posterolateral MI:
Tachyarrhythmias: Ventricular tachycardia and ventric-
ular fibrillation can occur similar to any acute MI during
the first few hours after onset of symptoms.
Left ventricular dysfunction: This can occur as a com-
plication if the artery is large and supplies a significant
portion of the myocardium.
AV block: AV can occur at the level of the AV node only if
the LCx coronary artery is dominant and there is associ-
ated inferior MI.
Anatomy and area supplied: The right coronary artery
(RCA) courses around the right or medial AV groove and
gives acute marginal branches to the right ventricle. The RCA
is the dominant artery in 85% to 90% of cases by continuing
posteriorly to the crux of the heart and giving rise to a
branch that supplies the AV node and the posterior descend-
ing artery, which supplies the inferior wall of the LV. The
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372 Chapter 23
RCA often continues beyond the crux toward the left AV
groove as the right posterior AV artery, which gives postero-
lateral branches to the LV.
Occlusion of the RCA:
Occlusion of the RCA will cause acute inferior MI with ST
elevation in II, III, and aVF.
ST elevation in V5 and V6 may occur because of postero-
lateral involvement of the LV.
Reciprocal ST depression in V1 to V3 with inferior MI sug-
gests the presence of a posterolateral MI. This can be veri-
fied by recording extra precordial leads V7, V8, and V9
which will show ST elevation consistent with a transmural
posterolateral MI (see LCx Coronary Artery Occlusion).
Acute inferior MI is usually due to occlusion of the RCA, ex-
cept in some patients where the LCx is the dominant artery.
Occlusion of the proximal RCA can cause right ventricular
infarction, which does not occur if the LCx coronary artery is
the culprit vessel. Inferior MI complicated by right ventricu-
lar infarction is a large infarct with a high mortality of 25%
to 30% compared with inferior MI without RV infarction,
which has a mortality of approximately 6%.
Acute inferior MI from occlusion of the RCA can be differ-
entiated from acute inferior MI due to occlusion of the LCx
coronary artery by the following ECG findings:
If ST elevation in lead III  lead II, the RCA is the culprit
vessel. This is based on the anatomical location of the
RCA, which circles the right AV groove and is closer to
lead III than lead II whereas the LCx circles the left AV
groove and is closer to lead II than lead III. Thus, if ST el-
evation in lead III  lead II, the proximal or mid RCA is
the culprit vessel, whereas if ST elevation in lead II  lead
III or ST elevation in III is not greater than II, the LCx ar-
tery is the culprit vessel.
ST depression in lead aVL  lead I, RCA is the culprit le-
sion. This is corollary to the observation mentioned pre-
viously, that lead III has a higher ST elevation when the
RCA is the culprit vessel. Because lead III is diametrically
opposite aVL, reciprocal ST depression will be more pro-
nounced in aVL than in lead I.
RV infarction can occur only if the proximal or mid RCA
is occluded (but not the LCx or distal RCA). The presence
of RV infarct is best diagnosed by recording right sided
precordial leads.
Complications of Acute Inferior MI:
VT and VF: This is similar to the complications of any
acute MI.
Bradyarrhythmias and AV block: Sinus bradycardia
and other sinus disturbances are very common findings
in acute inferior MI and are more common when the
RCA is involved. The RCA carries vagal afferent fibers,
which can cause sinus bradycardia due to reflex stimula-
tion rather than due to direct suppression of sinus node
function. Varying degrees of AV block (first, second, and
third degree) can occur with acute inferior MI. The AV
block is at the level of the AV node because the RCA sup-
plies the AV node in 85% to 90% of patients and by the
LCx in the remaining 10% to 15%. AV block at the level of
the AV node has a better prognosis than AV block occur-
ring in the distal conduction system. AV block occurring
during the first few hours of a myocardial infarct is usu-
ally due to a vagal mechanism and has a better prognosis
compared to AV block occurring late post-MI.
Intraventricular conduction defect: Intraventricular
conduction defect (IVCD), either RBBB or LBBB, may oc-
cur as a complication of acute MI. IVCD complicating
acute MI is usually associated with an extensive MI and
mortality is much higher when compared with patients
who do not develop IVCD. These patients have higher in-
cidence of asystole, AV block, VF, both primary and late,
as well as cardiogenic shock. The IVCD may be transient
or persistent. When the IVCD is transient, the prognosis
seems to be similar to patients who never developed the
conduction abnormality. Acute (new-onset) LBBB or a
previously existent (old) LBBB may conceal the ECG
changes of acute MI, whereas the ECG diagnosis of acute
MI can be recognized even when RBBB is present.
Atrial ischemia or infarction: Atrial branches to the
right atrium are usually supplied by the RCA which can
result in atrial ischemia or infarction when there is occlu-
sion of the proximal RCA. The acute onset of atrial fibril-
lation may be the only clue that atrial infarction had oc-
curred. Atrial infarction can also be diagnosed when
depression of the P-Q segment is present in the setting of
acute inferior MI.
Papillary muscle rupture: Most papillary muscle rupture
involves the posteromedial papillary muscle because it has
a single blood supply originating from the RCA. The an-
terolateral papillary muscle is less prone to rupture because
it has dual blood supply from the LAD and LCx coronary
arteries. Papillary muscle rupture is rare but is incompati-
ble with life because of acute severe mitral regurgitation.
RVMI: RVMI can occur only with acute inferior infarc-
tion due to occlusion of the proximal or probably mid-
RCA. It does not occur when the lesion involves the distal
RCA or LCx coronary artery.
n When acute inferior MI is diagnosed, RVMI should
always be routinely excluded by recording right-sided
precordial leads. The right-sided precordial leads
should be recorded immediately, because the ECG
changes in half of patients with RVMI may resolve
within 10 hours after the onset of symptoms. Right-
sided precordial leads are the most sensitive, most spe-
cific, and the least expensive procedure in the diagno-
sis of RVMI. ST elevation of 1 mm in any of the
right-sided precordial leads is diagnostic of RVMI
with lead V4R the most sensitive. Changes in the QRS
complex is not a criteria for the diagnosis of RVMI be-
cause the right ventricle does not contribute signifi-
cantly in the generation of the QRS complex.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
n If right-sided precordial leads were not recorded or
were recorded late during the course of the MI, the di-
agnosis of RVMI may be missed. Using the standard
12-lead ECG, RVMI is suspected when ST elevation in
lead III is greater than lead II (suggesting proximal
RCA occlusion) and ST elevation is present in V1.
n RVMI often presents with a special hemodynamic
subset of patients with acute MI who can develop the
clinical triad of hypotension, jugular neck vein disten-
sion, and clear lungs. This subset of patients can be
mistaken for cardiogenic shock. The presence of
Kussmaul sign characterized by distension of the neck
veins during inspiration is diagnostic of RVMI when
acute inferior MI is present. Approximately one third
to one half of patients with acute inferior MI have
RVMI but only 10% to 15% of patients with RVMI
will manifest the hemodynamic abnormality. The he-
modynamic picture of RVMI usually disappears after
a few weeks, suggesting that the RVMI is due to my-
ocardial stunning rather than necrosis. The thin-
walled right ventricle has a lower oxygen demand and
may partially receive its blood supply from the blood
within the right ventricular cavity, thus limiting the
extent of myocardial necrosis.
Treatment
The ECG remains the most useful test in planning the initial
strategies in the therapy of a patient with acute coronary syn-
drome. If a patient presents to a medical facility with symp-
toms of acute ischemia, the ACC/AHA guidelines recom-
mend that the ECG should be obtained and interpreted
within 10 minutes after patient entry. If ST elevation is pres-
ent in the initial ECG and patient is having symptoms due to
myocardial ischemia, 0.4 mg of sublingual nitroglycerin
should be given immediately, if not previously given, and re-
peated every 5 minutes for three doses. This is a Class I indi-
cation according to the ACC/AHA guidelines on ST eleva-
tion MI. Nitroglycerin is helpful in excluding vasospasm as
the cause of the ST segment elevation. If the ST elevation
persists after three successive doses, immediate reperfusion
of the occluded artery with a thrombolytic agent or with pri-
mary PCI should be considered without waiting for the re-
sults of cardiac troponins. Although acute coronary syn-
drome with ST segment elevation is almost always associated
with increased troponins in the circulation, the troponins
may not be elevated in some patients presenting to the hos-
pital within 6 hours after symptom onset.
Thrombolytic therapy: Thrombolytic therapy or primary
PCI should be considered if the chest pain is at least 20 min-
utes in duration.
The following are the ECG criteria for immediate throm-
bolytic therapy or PCI:
n ST elevation 1 mm is present in any two adjacent
leads.
373
n New or presumably new-onset LBBB associated with
symptoms of ischemia.
n ST segment depression even in the presence of cellular
necrosis (elevated cardiac troponins) is not an indica-
tion for thrombolytic therapy. The only exception is ST
segment depression in V1 to V3, which may represent a
straight posterior or posterolateral infarct. A posterior
infarct is a transmural infarct and can be verified by
the presence of ST elevation in leads V7 to V9.
Virtually all myocardial cells supplied by the infarct re-
lated artery become necrotic within 6 hours after symp-
tom onset, unless collateral flow is adequate. Thus, if
thrombolytic therapy is elected, it should be given within
30 minutes after patient entry to the emergency depart-
ment (door to needle time) or first contact with emer-
gency personnel (medical contact to needle time).
Thrombolytic therapy is most effective when given within
2 hours after symptom onset. With further delay, the ben-
efits of any type of reperfusion therapy decline.
The therapeutic window for thrombolytic therapy is up to
12 hours after symptom onset. This may be extended to
24 hours for some patients who continue to have stutter-
ing symptoms of chest pain with persistent ST elevation.
Absolute contraindications to thrombolytic therapy accord-
ing to the 2004 ACC/AHA guidelines include: any prior in-
tracranial hemorrhage, known structural cerebrovascular
lesion such as arteriovenous malformation, known malig-
nant intracranial neoplasm either primary or metastatic, is-
chemic stroke within 3 months, suspected aortic dissection,
active bleeding or bleeding diathesis other than menses, and
significant closed head or facial trauma within 3 months.
Relative contraindications include history of chronic se-
vere, poorly controlled hypertension, severe uncon-
trolled hypertension on presentation (systolic blood
pressure 180 mm Hg or diastolic blood pressure 110
mm Hg), history of prior ischemic stroke 3 months,
dementia or known intracranial pathology that is not in-
cluded under absolute contraindications, traumatic or
prolonged cardiac resuscitation 10 minutes, major sur-
gery 3 weeks, recent (within 2 to 4 weeks) internal
bleeding, noncompressible vascular punctures, preg-
nancy, active peptic ulcer, current use of anticoagulants
(the higher the International Normalized Ratio, the
higher the risk of bleeding), and prior exposure (5
days) to streptokinase/anistreplase or prior allergic reac-
tion to these agents.
Intracerebral hemorrhage is a major complication and is
expected to occur in approximately 1% of patients receiv-
ing thrombolytic therapy. It is fatal in up to two thirds of
patients with this complication. Patients older than 65
years, a low body weight of 70 kg, and alteplase (as op-
posed to streptokinase) as the thrombolytic agent, are asso-
ciated with higher incidence of intracerebral hemorrhage.
There are five thrombolytic agents approved for intravenous
use: (1) tissue plasminogen activator or tPa (alteplase),
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374 Chapter 23
(2) recombinant tissue plasminogen activator or rtPa
(reteplase), (3) tenecteplase, (4) streptokinase, and (5)
anistreplase. Alteplase, reteplase, and tenecteplase are plas-
minogen activators. These are selective agents that specifi-
cally convert plasminogen to plasmin and are given
concomitantly with intravenous heparin infusion. Streptok-
inase and anistreplase do not require heparin infusion be-
cause these nonselective thrombolytic agents can cause de-
pletion of the coagulation factors and produce massive
amounts of fibrin degradation products, which have antico-
agulant properties. If patient is a high risk for systemic em-
boli such as the presence of a large infarct, atrial fibrillation,
left ventricular thrombus, or previous embolus, Activated
partial thromboplastin time should be checked 4 hours after
these nonselective thrombolytic agents have been given and
heparin started when activated partial thromboplastin time
is 2 times control (or 70 seconds).
Additional medical therapy for ST elevation MI include:
Aspirin: The initial dose of aspirin is 162 to 325 mg
orally. This should be given immediately even before the
patient arrives to a medical facility. Plain aspirin (not en-
teric coated), should be chewed. Maintenance dose of 75
to 162 mg daily is continued indefinitely thereafter.
n If the patient is allergic to aspirin, clopidogrel should
be given as a substitute.
n In patients undergoing coronary bypass surgery, as-
pirin should be started within 48 hours after surgery
to reduce closure of the saphenous vein grafts.
n Patients who have PCI with stents placed should ini-
tially receive the higher dose of aspirin at 162 to 325 mg
daily for one month for bare metal stent, 3 months for
sirolimus and 6 months for paclitaxel eluting stent and
continued at a dose of 75 to 162 mg daily indefinitely.
Clopidogrel: Similar to aspirin, clopidogrel is considered
standard therapy and is a Class I recommendation in pa-
tients with acute coronary syndrome including patients
with ST elevation MI with or without reperfusion therapy
according to the 2007 focused update of the ACC/AHA
2004 guidelines for ST elevation MI. The maintenance
dose is 75 mg orally daily for a minimum of 14 days and
reasonably up to a year. The loading dose is 300 mg orally,
although in elderly patients 75 years especially those
given fibrinolytics, the loading dose needs further study.
n In patients undergoing coronary bypass surgery,
clopidogrel should be discontinued at least 5 days and
preferably for 7 days unless the need for surgery out-
weighs the risk of bleeding.
Unfractionated heparin: When unfractionated heparin
is given concomitantly with a selective thrombolytic agent
such as tPA, rtPA, or tenecteplase, the recommended dose
is 60 U/kg given as an IV bolus. The initial dose should not
exceed 4,000 U. This is followed by a maintenance dose of
40% and patients with hypertension, dia-
12 U/kg/hour not to exceed 1,000 U/hour for patients
weighing more than 70 kg. Activated partial thromboplas-
tin time should be maintained to 50 to 70 seconds or 1.5 to
2 times baseline. Heparin is usually given for 48 hours, but
may be given longer if there is atrial fibrillation, left ven-
tricular thrombi, pulmonary embolism, or congestive
heart failure. Platelets should be monitored daily. When
given to patients not on thrombolytic therapy, the dose is
60 to 70 U/kg bolus followed by maintenance infusion of
12 to 15 U/kg/hour. According to the ACC/AHA 2007 re-
vised guidelines on unstable angina and non-ST elevation
MI, patients who did not receive thrombolytic therapy
may receive other types of heparin other than unfraction-
ated heparin for the whole duration of hospitalization or
for a total of 8 days. This includes low-molecular-weight
heparin (enoxaparin) and fondaparinux.
n Enoxaparin: An initial 30 mg IV bolus is followed by a
subcutaneous injection of 1 mg/kg every 12 hours. For
patients older than 75 years of age, the initial bolus is
omitted and the subcutaneous dose is 0.75 mg/kg every
12 hours. The dose should be adjusted if the serum crea-
tinine is 2.5 mg/dL in men and 2.0 mg/dL in women.
n Fondaparinux: The initial dose is 2.5 mg IV followed
by subcutaneous doses of 2.5 mg once daily up to the
duration of hospitalization or a maximum of 8 days
provided that the creatinine is 3.0 mg/dL.
Nitroglycerin: Nitroglycerin is initially given sublin-
gually unless the patient is hypotensive with a blood pres-
sure 90 mm Hg or heart rate is 50 bpm or there is sus-
pected RVMI. Intravenous nitroglycerin is given when
there are symptoms of ongoing ischemia or congestive
heart failure or for uncontrolled hypertension.
Oxygen: Oxygen supplementation is given to improve
arterial saturation.
Morphine sulfate: Morphine sulfate is the analgesic of
choice with a Class I recommendation for pain relief for ST
elevation MI but only a Class IIa recommendation for non-
ST elevation MI. The dose is 2 to 4 mg IV and repeated in
increments of 2 to 8 mg at 5- to 15-minute intervals.
Beta blockers: Beta blockers should be given orally in the
first 24 hours unless the patient has contraindications to
beta blocker therapy such as PR interval 0.24 seconds,
second-degree AV block or higher, signs of heart failure, or
low cardiac output and bronchospastic pulmonary disease.
This is given a Class I recommendation in the ACC/AHA
guidelines. Beta blockers have been shown to decrease the
incidence of ventricular arrhythmias after acute MI. Beta
blockers may be administered IV if hypertension is present.
This carries a Class IIa recommendation.
Antagonists of the renin-angiotensin system: The use
of angiotensin-converting enzyme inhibitors is a Class I
recommendation in patients with ST elevation MI. It
should be given orally (not IV) and continued indefinitely
in patients with ST elevation MI with left ventricular ejec-
tion fraction
betes, or chronic renal disease in the absence of con-
traindications to angiotensin-converting enzyme inhibitor
therapy. Angiotensin receptor blockers, specifically valsartan
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
or candesartan, may be given if the patient cannot tolerate
angiotensin-converting enzyme inhibitors. The routine use
of angiotensin-converting enzyme inhibitors or an-
giotensin receptor blockers is reasonable in patients with
acute ST elevation MI without any of the above indica-
tions. This carries a Class IIa recommendation.
Aldosterone antagonist: Aldosterone antagonists
(eplerenone in post-MI patients and spironolactone in
patients with chronic heart failure), have been shown to
reduce mortality. The 2007 focused update of the
ACC/AHA 2004 guidelines on ST elevation MI gives a
Class I recommendation for the use of aldosterone block-
Facilitated PCI: This involves the administration of heparin
ers to patients with ejection fraction of
40% and have
either diabetes or heart failure unless there is renal dys-
function (serum creatinine 2.5 mg/dL in men and 2.0
mg/dL in women and potassium 5.0 mEq/L).
Cholesterol-lowering agents: Statins or if contraindi-
cated, other lipid-lowering agents, should be given to
lower low-density lipoprotein cholesterol to 100 mg/dL
in all patients and further lowering to 70 mg/dL is rea-
sonable in some patients.
IIB/IIIA inhibitors: Other antiplatelet agents such as
IIB/IIIA inhibitors (abciximab, eptifibatide, and tirofiban)
are not indicated in the treatment of ST elevation MI un-
less the patient is being readied for primary PCI. The use
of standard dose IIB/IIIA inhibitor (abciximab) in com-
bination with half-dose thrombolytic agent (reteplase)
Cardiac pacemakers and acute MI:
has not been shown to improve mortality in the short
term (30 days) or long term (1 year) compared with the
use of the thrombolytic agent alone.
Primary PCI: Primary PCI is the most effective reperfusion
method and has now become the standard therapy for reper-
fusing ST elevation MI in centers that are capable of doing
the procedure in a timely fashion. The success rate of being
able to reperfuse the occluded artery with primary PCI is
90%, whereas the 90-minute patency rate with throm-
bolytic therapy is approximately 65% to 75%. Unfortunately,
PCI can be performed only in centers with interventional
cardiac catheterization laboratories, and in some states, only
when backup cardiac surgery is available. The most recent
2007 focused update of the ACC/AHA guidelines on ST ele-
vation MI reemphasizes the previous recommendation that
reperfusion of the occluded artery should be started as early
as possible since the greatest benefit of any type of reperfu-
sion therapy depends on the shortest time in which complete
reperfusion is achieved. Therefore, the delay in performing
PCI should be considered when deciding whether throm-
bolytic therapy or primary PCI is the best modality of reper-
fusion. Thus, if the patient is admitted to a hospital that is ca-
pable of doing PCI, the procedure should be performed
within 90 minutes after first medical contact. If the patient is
admitted to a facility that is not capable of doing PCI and it
is not possible to perform PCI within 90 minutes with inter-
hospital transfer, thrombolytic therapy should be given unless
contraindicated, within 30 minutes of hospital presentation.
375
Transfer to another hospital with PCI capabilities should be
considered when:
Thrombolytic therapy is contraindicated.
PCI can be performed within 90 minutes (door to balloon
time) of first medical contact.
Thrombolytic therapy had been tried but failed to reper-
fuse the occluded artery (rescue PCI).
PCI is also the therapy of choice when the patient is hemo-
dynamically unstable especially when there is cardiogenic
shock or pump failure, onset of symptoms is more than 3
hours or the diagnosis of ST elevation MI is in doubt.
in high doses, IIb/IIIa antagonists, fibrinolytic agents in less
than full doses or a combination of the agents discussed pre-
viously before PCI is attempted. Full dose thrombolytic ther-
apy followed by immediate PCI may be harmful and is not
recommended (Class III recommendation according to the
2007 focused update ACC/AHA 2004 guidelines for the
management of patients with ST elevation MI). These an-
tithrombotic agents are given to improve patency of the oc-
cluded coronary artery. Facilitated PCI is performed if pri-
mary PCI is not available within 90 minutes after first
medical contact. This is usually performed when the patient
is initially admitted to a hospital without PCI capabilities
and interhospital transfer is being planned to a facility that is
capable of doing PCI.
In patients with acute MI complicated by AV block, im-
plantation of permanent pacemakers depends on the lo-
cation of the AV block (which should be infranodal),
rather than the presence or absence of symptoms. Most
patients with infranodal block have wide QRS complexes.
However, when AV block is persistent and is associated
with symptoms, the AV block may or may not be infran-
odal before a permanent pacemaker is implanted.
Whenever a patient who has survived an acute MI be-
comes a candidate for permanent pacemaker, two other
conditions should be answered. These include the need for
biventricular pacing because most of these patients will
have an intraventricular conduction defect and the need
for implantable cardioverter defibrillator (ICD) because
most of these patients have left ventricular dysfunction.
Indications of implantation of permanent pace-
maker after acute MI: The following are indications for
insertion of a permanent pacemaker following acute ST
elevation MI according to the ACC/AHA/Heart Rhythm
Society (HRS) 2008 guidelines for device-based therapy
of cardiac rhythm abnormalities and the ACC/AHA 2004
guidelines for the management of ST elevation MI.
n Class I recommendation:
n Persistent second-degree AV block in the His-
Purkinje system with bilateral bundle-branch
block or third-degree AV block within or below the
His-Purkinje system.
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376 Chapter 23
n Transient advanced second- or third-degree AV
block at the infranodal level and associated bundle
branch block. An electrophysiologic study may be
necessary if the site of the block is uncertain.
n Persistent and symptomatic second- or third-
degree AV block.
n Class IIb recommendation:
n Persistent second- or third-degree AV block at the
level of the AV node.
n Class III recommendation: permanent pacing is not
recommended in the following conditions:
n Transient AV block without intraventricular con-
duction defect.
n Transient AV block in the presence of isolated left
anterior fascicular block.
n Acquired left anterior fascicular block in the ab-
sence of AV block.
n Persistent first-degree AV block in the presence of
bundle branch block, old or indeterminate.
Ventricular and supraventricular tachycardia: The
treatment of ventricular and supraventricular tachycardia
following acute MI is similar to the general management of
these arrhythmias in patients without ischemic heart
disease.
Implantation of ICD after acute MI: In patients with acute
MI, the following are indications for implantation of ICD ac-
cording to the ACC/AHA 2004 guidelines for the manage-
ment of ST elevation MI:
Class I recommendation:
n Patients with VF or hemodynamically significant VT
more than 2 days after acute MI not from reversible is-
chemia or from reinfarction.
n Left ventricular ejection fraction of 31% to 40% at
least 1 month after acute MI even in the absence of
spontaneous VT/VF or have inducible VT/VF on elec-
trophysiological testing.
Class IIa recommendation:
n Left ventricular dysfunction (ejection fraction
30%)
at least 1 month after acute MI and 3 months after
coronary artery revascularization.
Class IIb recommendation:
n Left ventricular dysfunction (ejection fraction 31% to
40%) at least 1 month after acute ST elevation MI
without additional evidence of electrical instability
such as nonsustained VT.
n Left ventricular dysfunction (ejection fraction 31% to
40%) at least 1 month after acute ST elevation MI and
additional evidence of electrical instability such as
nonsustained VT but do not have inducible VF or sus-
fained VT on electrophysiologi testing.
Class III recommendation: ICD is not indicated when
ejection fraction is 40% at least 1 month after acute ST
elevation MI.
RVMI: Left ventricular preload may be diminished from
right ventricular failure and volume is needed to optimize
diastolic filling and cardiac output. Treatment of RVMI
therefore usually requires adequate hydration with IV
fluids.
The use of nitroglycerin may further reduce preload
and potentiate the hemodynamic abnormalities associ-
ated with RVMI and should be used cautiously when
acute inferior MI is present. It is contraindicated if
systolic blood pressure is 90 mm Hg or heart rate is
50 bpm.
Acute inferior MI complicated by RVMI involves not only
the right ventricle but may be associated with significant
left ventricular dysfunction. If left ventricular output is
low and LV filling pressure is high (high pulmonary
wedge pressure), inotropic support with dopamine or
dobutamine should be considered.
Complete AV block may occur as a complication of
RVMI because the artery to the AV node is usually com-
promised when there is occlusion of the proximal or
mid-RCA. If the AV block is associated with a low ven-
tricular rate of 50 bpm or patient is hemodynamically
unstable with low output, atropine is the drug of choice.
The dose is 0.5 to 1.0 mg IV repeated every 3 to 5 minutes
until a total dose of 3 mg (0.04 mg/kg) is given within a
period of 3 hours. This dose can result in complete vagal
blockade and need not be exceeded. Doses of 0.5 mg
should be discouraged because it may slow instead of in-
crease heart rate by stimulation of the vagal nuclei cen-
trally resulting in parasympathomimetic response. If AV
block does not respond to atropine, temporary dual
chamber pacing to preserve AV synchrony may be
needed to optimize left ventricular output because ven-
tricular performance is dependent on atrial contribution
to left ventricular filling.
Prognosis
Acute MI continues to be the leading cause of death and dis-
ability in spite of the advances in the diagnosis and therapy of
coronary disease. About half of all deaths from acute MI will
occur during the initial hours after the onset of symptoms
with most deaths from ventricular fibrillation. Most deaths
occur before the patients are able to reach a medical facility.
Of those who survive and are able to seek medical care, prog-
nosis is dependent on the extent and severity of myocardial
damage.
ST elevation MI is more extensive than non-ST elevation MI
resulting in a lower ejection fraction, higher incidence of
heart failure, ventricular arrhythmias, and higher immedi-
ate and in-hospital mortality of up to 10% compared with
non-ST elevation MI, which has a lower incidence of the
above complications and a lower in-hospital mortality of
1% to 3%.
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Acute Coronary Syndrome: ST Elevation Myocardial Infarction
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Acute Coronary Syndrome:
Non-ST Elevation Myocardial
Infarction and Unstable Angina
Acute coronary syndrome: Acute coronary syn-
drome is usually from plaque rupture, resulting in
varying degrees of myocardial ischemia. The electro-
cardiogram (ECG) provides useful information that
cannot be obtained with other diagnostic procedures
and is the most important modality in the initial man-
agement of patients with this disorder.
ECG findings: Patients with acute coronary syndrome
can be classified according to their ECG presentation
and include those with ST segment elevation and those
without ST elevation.
ST elevation: Almost all patients with acute coro-
nary syndrome with ST segment elevation will de-
velop myocardial necrosis with increased cardiac
troponins in the circulation. These patients have an
occluded coronary artery with completely ob-
structed flow and are candidates for immediate
reperfusion with a thrombolytic agent or with pri-
mary percutaneous coronary intervention (PCI).
This was discussed in Chapter 23, Acute Coronary
Syndrome: ST Elevation Myocardial Infarction.
Non-ST elevation: Patients with acute coronary syn-
drome without ST segment elevation usually have ST
depression, T-wave inversion, or less-specific ST and
T wave abnormalities. Some patients may not show
any changes in the ECG. These patients will either
have unstable angina with no evidence of myocardial
necrosis or non-ST elevation myocardial infarction
(MI) when evidence of myocardial necrosis is pres-
ent. The presence or absence of myocardial necrosis is
based on whether or not cardiac troponins are ele-
vated in the circulation. Unstable angina and non-ST
elevation MI have the same pathophysiology, similar
ECG findings, similar clinical presentation, and simi-
lar management and are discussed together.
The ECG is also helpful in providing prognostic infor-
mation in acute coronary syndrome based on the ini-
tial presentation.
24
Patients with acute coronary syndrome accompa-
nied by ST segment elevation carries the highest risk
of death during the acute phase.
Patients presenting with ST segment depression have
the highest overall mortality over a period of 6 months.
Patients with isolated T wave inversion or those with
no significant ECG abnormalities incur the lowest risk.
The Normal T Wave
The normal T wave: The T wave normally follows the
direction of the QRS complex. Thus, in leads where
the R waves are tall, the T waves are also tall. In leads
where the S waves are deep and the R waves are small,
as in leads III or aVL, the T waves may be flat or in-
verted. Determining the direction or axis of any wave
in the ECG such as the QRS complex was previously
discussed in Chapter 4, The Electrical Axis and Car-
diac Rotation.
Frontal plane: In the frontal plane, the axis of the
normal T wave is within 45 of the axis of the QRS
complex (Figs. 24.1 and 24.2). This is also called the
QRS/T angle, which is the angle formed between the
axis of the QRS complex and that of the T wave.
When this angle is increased, myocardial ischemia
should be considered, although this is usually not a
specific finding. The tallest T wave in the limb leads
is approximately 5 mm but could reach up to 8 mm.
Horizontal plane: In the horizontal plane, the axis
of the normal T wave is within 60 of the axis of the
QRS complex. Calculation of the T-wave axis in the
horizontal plane is usually not necessary, because
the T waves are expected to be upright in most pre-
cordial leads other than V1 or V2. If the T waves are
inverted in V1, V2, and also in V3, this is abnormal
(Fig. 24.3), except in children and young adults.
379
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380 Chapter 24
aVR
-150 aVL - 30
I 0
+15
+30
III+120 II +60
aVF
+105 +90 +60 QRS
Figure 24.1: Axis of the T Wave in the Frontal Plane. If
the axis of the QRS is 60, the T wave should be within 45 (shaded)
to the left or right of the axis of the QRS complex as shown.
Because the precordial leads are closer to the heart
than the limb leads, the T waves are taller in the pre-
cordial leads, especially V2V4, and usually measure
up to 10 mm but can reach up to 12 mm.
The normal T wave:
In Figure 24.2, the axis of the T wave and QRS com-
plex is almost 0. Although the T wave is inverted in
lead III (arrows), this is not abnormal because the
axis of the T wave is within 45 of the axis of the QRS
complex. In the horizontal plane, the T wave is in-
verted in V1 and upright in V2 to V6. This is also a
normal finding.
In Figure 24.3, the T waves are inverted in V1, V2 and
V3 (arrows). This is abnormal in adults. However,
inversion of the T wave from V1 to V3 is entirely nor-
mal in children. This T-wave inversion may nor-
mally persist through adulthood in some patients
and is called persistent juvenile pattern.
Abnormal T Waves
T waves: Figure 24.4 shows different examples of T
waves, both normal and abnormal.
Figure 24.2:T Wave Axis in the
Frontal Plane. Although the T
waves are inverted in lead III (arrows),
the axis of the T wave is within 45 of
the axis of the QRS complex (QRS
axis 0, T wave axis 5), thus the T
wave inversion in lead III is expected.
This is not an abnormal finding.
Normal T wave: A normal T wave is upright and
asymmetric. The initial upstroke is inscribed slowly
and the terminal downstroke is inscribed more rap-
idly (Fig. 24.4A).
Ischemic T waves: Figure 24.4BD show typical is-
chemic T waves. Ischemic T waves are symmetrical.
They are symmetrically tall when the ischemia is
subendocardial and are deeply symmetrically in-
verted, measuring at least 2 mm when the ischemia
is subepicardial or transmural. These T-wave abnor-
malities when accompanied by symptoms of my-
ocardial ischemia may or may not be associated with
troponin elevation.
Nonspecific T waves: The other T-wave abnormal-
ities shown in Figure 24.4EG are nonspecific.
These include T waves that are inverted but are 2
mm in amplitude. They may nevertheless occur as
the only ECG abnormality associated with acute
myocardial ischemia and may or may not be associ-
ated with troponin elevation. It is also possible that
the ECG may not show any definite abnormalities
when there is myocardial ischemia.
Interpretation of any T-wave abnormality should al-
ways include all available clinical information be-
cause the T-wave abnormalities are not always from
ischemia, even if they look typical for myocardial
ischemia.
Abnormal T-wave changes from myocardial
ischemia: When coronary blood flow is diminished or
when myocardial oxygen demand exceeds blood sup-
ply, changes in the T waves are the earliest to occur.
Electrocardiographically, changes confined to the T
waves indicate myocardial ischemia, which may be
subendocardial or transmural.
Subendocardial ischemia: Myocardial ischemia is
subendocardial when it is localized to the subendo-
cardial area. It is usually manifested in the ECG as
peaking of the T waves over the area of ischemia.
Transmural ischemia: The ischemia is transmural
or subepicardial when it involves the whole thick-
ness of the myocardium. This is usually manifested
in the ECG as deeply and symmetrically inverted T
waves over the area of ischemia.
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina
Subendocardial ischemia: The typical pattern of
subendocardial ischemia is the presence of tall and sym-
metrically peaked T waves (Fig. 24.5). The configura-
tion of the T wave is similar to that of hyperkalemia ex-
cept that in subendocardial ischemia, the base is usually
broad and the QT interval is slightly prolonged. Peaking
of the T waves is confined to the area of ischemia unlike
hyperkalemia where peaking is generalized (Fig. 24.6).
Peaking of the T waves may also occur in fluoride intox-
ication and left ventricular hypertrophy from volume
overload such as aortic regurgitation. It can also occur
as a normal finding (Fig. 24.7) or when there is a meta-
bolic abnormality (Fig. 24.8) especially over the precor-
dial transition zone V2 to V4. Thus, peaking of the T
wave is not specific for myocardial ischemia.
Transmural ischemia: T waves that are symmetrically
and deeply inverted may indicate transmural ischemia,
which involves the whole thickness of the myocardium.
In transmural or subepicardial ischemia, the T wave is
pointed downward, often resembling an arrowhead. If
the T wave is divided equally into two halves by draw-
ing a perpendicular line at the middle of the T wave,
the left half of the inverted T wave resembles the other
A B C D
E F G hemorrhage. Deep T-wave inversion is noted in the
Figure 24.4: T Waves. (A) Normal T wave. (B) Peaked T
waves from subendocardial ischemia. (C) Classical deep T-wave
inversion due to transmural ischemia. (D) Symmetrically but less
deeply inverted T wave also due to transmural ischemia. (E)
Shallow T-wave inversion (F) Biphasic T wave. (G) Low, flat, or iso-
electric T wave. Although the T-wave configuration of B, C, and
D suggests myocardial ischemia, these T-wave abnormalities
may also be due to other causes.
381
Figure 24.3: Persistent Juvenile
Pattern. The electrocardiogram is
from a 25-year-old asymptomatic fe-
male showing inversion of the T
wave in V1 to V3 (arrows). This is a nor-
mal finding in children, which may
normally persist to adulthood and is
called persistent juvenile pattern.
half. The ST segment may or may not be depressed.
The QTc may be slightly prolonged (Fig. 24.9). When
acute symptoms of ischemia are also present, these T
waves may or may not be associated with troponin ele-
vation. When troponins are elevated in the circulation,
non-ST elevation MI or more specifically a T-wave in-
farct is present; otherwise, the T wave changes are due
to unstable angina.
Other causes of deep T-wave inversion: There are
several other causes of deep and symmetrical T-wave in-
version other than myocardial ischemia. These include
hypertrophic cardiomyopathy especially the apical type,
pericarditis, pulmonary embolism, mitral valve prolapse,
metabolic conditions, electrolyte disorders, and effect of
drugs such as tricyclic antidepressants and antiarrhyth-
mic agents. It can also be due to noncardiac conditions
such as cerebrovascular accidents or other craniocerebral
abnormalities, peptic ulcer perforation, acute cholecysti-
tis, and acute pancreatitis. It may even be a variant of nor-
mal especially in young African American males. Deep
symmetrical inversion of the T wave, therefore, is not
specific and does not necessarily imply that the T-wave
abnormality is due to transmural myocardial ischemia.
Figure 24.10 is the initial ECG of a patient who pre-
sented with chest discomfort. There was deep and
symmetrical T-wave inversion across the pre-
cordium. The cardiac troponins were elevated con-
sistent with non-ST elevation MI or, more specifi-
cally, a T-wave infarct.
Figure 24.11 is the 12-lead ECG of a 37-year-old
woman, without history of cardiac disease and is 6
months postpartum when she developed cerebral
limb and precordial leads resembling transmural is-
chemia.
Secondary ST and T wave abnormalities: The ab-
normality in the T wave as well as the ST segment is
secondary if it is caused by abnormal depolarization of
the ventricles, as would occur when there is bundle
branch block, ventricular hypertrophy, preexcitation of
the ventricles, or when the rhythm is ectopic or in-
duced by a ventricular pacemaker. These secondary ST
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382 Chapter 24

Figure 24.5: Subendocardial Ischemia. Peaking of the T waves is confined to V1 to V4

consistent with subendocardial ischemia involving the anterior wall. Note also that the T
waves are taller in V1 than in V6 and are biphasic in leads II, III, and aVF. Peaking of the T waves
mark the area of ischemia and can occur as the initial manifestation of acute coronary
syndrome before the onset of ST segment elevation.

Figure 24.6: Hyperkalemia.

Peaking of the T waves from hyper-
kalemia (serum potassium  6.6
mEq/L). In subendocardial ischemia,
the abnormally peaked T waves are
localized to the ischemic area. In hy-
perkalemia, peaking of the T waves is
generalized (arrows).

Figure 24.7: Peaked T Waves.

Routine electrocardiogram obtained
from an asymptomatic middle-age
male. Peaked T waves are present
representing a normal variant.
Peaked T waves are often associated
with early repolarization. Potassium
level was 3.8 mEq/L.

Figure 24.8: Giant T Waves.

Twelve-lead electrocardiogram (ECG)
of a 33-year-old alcoholic man show-
ing giant T waves with prolonged
QTc. The T waves are tall and peaked
with a broad base. The cause of the
ECG abnormality was thought to be
due to alcohol or associated
metabolic abnormality.
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina
and T-wave abnormalities are therefore associated with
abnormal QRS complexes, unlike myocardial ischemia,
which is a primary repolarization disorder. Figures
24.12 and 24.13 are examples of secondary ST and
T-wave abnormalities. In Figure 24.12, the T waves are
inverted because of left ventricular hypertrophy; in
Figure 24.13, from preexcitation of the ventricles.
Mechanism of Normal and Abnormal
T Waves
Normal myocardium: Because the Purkinje fibers are
located subendocardially, depolarization of the my-
ocardium is endocardial to epicardial in direction. A
surface electrode overlying the myocardium will
The ST Segment
record a tall QRS complex. Although the epicardium is
the last to be depolarized, it is the earliest to recover
because it has the shortest action potential duration
when compared to other cells in the myocardium. Be-
cause the direction of repolarization is epicardial to
endocardial, this causes the T wave to be normally up-
right (Fig. 24.14A).
Myocardial ischemia: Myocardial ischemia may alter
the direction of repolarization depending on the sever-
ity of the ischemic process. This will cause changes that
are confined to the T waves.
383
Figure 24.9:Transmural
Myocardial Ischemia. The T-
wave changes shown are typical of
transmural ischemia. Ischemic T
waves are deeply inverted, usually
measuring 2 mm and resemble the
tip of an arrowhead as shown in V3
to V6.
Subendocardial ischemia: When myocardial is-
chemia is confined to the subendocardium, the
direction of depolarization and repolarization is not
altered and is similar to that of normal myocardium.
The repolarization wave however is delayed over the
area of ischemia causing the T wave to become taller
and more symmetrical (Fig. 24.14B). These changes
are confined to the ischemic area.
Transmural ischemia: When the whole thickness
of the myocardium is ischemic, the direction of the
repolarization wave is not only reversed that of nor-
mal but also travels slowly causing the T wave to be
deeply and symmetrically inverted (Fig. 24.14C).
The normal ST segment is isoelectric and is at the same
level as the TP and PR segments. The ST segment is ab-
normal when it is elevated or depressed by 1 mm
from baseline or the configuration changes into a dif-
ferent pattern. Electrocardiographically, alteration in-
volving the ST segment indicates a more advance stage
of myocardial ischemia and is called myocardial injury.
ST elevation: Acute coronary syndrome with ST
elevation indicates that one of the three epicardial
coronary arteries is totally occluded with TIMI 0 flow
Figure 24.10: T-Wave Inversion
from non-ST Elevation MI. The
T waves are symmetrically and
deeply inverted in most leads. These
electrocardiogram changes are asso-
ciated with elevation of the cardiac
troponins consistent with non-ST
elevation myocardial infarction or,
more specifically, a T-wave infarct.
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384 Chapter 24

Figure 24.11: T-Wave Inversion from Cerebrovascular Accident Hemorrhage.

The electrocardiogram (ECG) is from a 37-year-old woman 6 months postpartum who devel-
oped a left occipital hemorrhage. Note that the T-wave inversion is deep and symmetrical in
V2 to V6 and also in leads I, II, and aVF resembling transmural myocardial ischemia. Note the
similarity of this ECG from that in Figure 24.10.

Figure 24.12: Secondary ST and T-Wave Abnormality. The electrocardiogram

shows left ventricular hypertrophy. Tall R waves are present with downsloping ST depression
and T wave-inversion (arrows). These ST-T changes are secondary to abnormal activation of
the ventricles.

Figure 24.13: Secondary T-

Wave Abnormality. Twelve-lead
electrocardiogram showing preexci-
tation. The ST-T abnormalities
(arrows) are secondary to abnormal
activation of the ventricles.
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina 385

Depolarization Depolarization
Depolarization

Endo-

Epi-
Repolarization Repolarization Repolarization

A: Normal Myocardium B: Subendocardial Ischemia C: Transmural Ischemia

Figure 24.14: (A) The T Wave Normal myocardium. Depolarization starts from endocardium to epi-
cardium since the Purkinje fibers are located subendocardially. Repolarization is reversed and is epicar-
dial to endocardial, thus the T wave and QRS complex are both upright. (B) Subendocardial Ischemia.
The shaded portion represents the area of ischemia. The direction of depolarization and repolarization is
similar to normal myocardium. After the repolarization wave reaches the ischemic area, the
repolarization wave is delayed causing the T wave to be tall and symmetrical. (C) Transmural Ischemia.
The direction of repolarization is reversed that of normal and is endocardial to epicardial resulting in
deeply and symmetrically inverted T waves.

indicating no perfusion or antegrade flow beyond the
point of occlusion. Thrombotic occlusion of the vessel
lumen with ST segment elevation almost always results
in cellular necrosis with elevation of the cardiac tro-
ponins in the circulation. ST elevation electrocardio-
graphically indicates transmural or subepicardial injury,
which involves the whole thickness of the myocardium.
ST depression: ST depression from acute coronary
syndrome electrocardiographically indicates suben-
docardial myocardial injury. Unlike ST elevation,
which is almost always accompanied by cellular
necrosis, ST depression may or may not be associated
with troponin elevation. ST depression may be hori-
zontal (Fig. 24.15A,B), downsloping (C,D), scooping
(E), slow upsloping (F), or fast upsloping (G). Typical
ST depression from subendocardial injury is usually
horizontal (A,B), downsloping (C), or slow upsloping
(F) accompanied by depression of the J point. These
types of ST segment depression, however, may be
caused by other conditions that may be cardiac or
noncardiac and similar to T-wave inversion, are not
specific for myocardial injury.
The typical ST depression associated with acute coro-
nary syndrome has a horizontal or downsloping con-
figuration with depression of the J point of at least
1 mm as shown in Figures 24.15AC, 24.16, and 24.17.
Other types of ST segment depression are less specific.
Unlike ST elevation, ST depression from acute myocar-
dial injury, even when accompanied by troponin eleva-
tion, is not an indication for thrombolytic therapy. It
usually indicates multivessel coronary disease, includ-
ing significant stenosis of the left main coronary artery.

A B C D E F G

Figure 24.15: ST Segment Depression. (A, B) Horizontal ST depression. (C, D)

Downsloping ST segment depression. (E) Scooping ST segment depression frequently
from digitalis effect. (F) Slow upsloping ST segment depression. (G) Fast upsloping ST seg-
ment depression frequently a normal finding. (A, B, C, F) Typical ischemic ST depression.
(D) Left ventricular strain frequently associated with left ventricular hypertrophy. Arrows
indicate the J point.
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386 Chapter 24

Figure 24.16: ST Segment De-

pression. Horizontal ST depression
is seen in leads I and II and horizontal
to downsloping ST depression in V3
to V6 consistent with subendocardial
injury. Serial troponins were not ele-
vated and the patients symptoms
were consistent with unstable
angina.

cated. This type of ST segment depression may also oc-

ST Segment Depression
ST depression in V1 to V3: Acute coronary syndrome
with ST segment depression in the ECG is a contraindi-
cation to thrombolytic therapy. One exception is ST seg-
ment depression in V1 to V3, which may represent a true
posterolateral ST elevation MI from total occlusion of the
left circumflex coronary artery (Fig. 24.17). When ST
segment depression is present in V1 to V3, special leads V7
to V9 should be recorded to exclude a true posterolateral
MI, which represents a true ST elevation MI. This has
been previously discussed in Chapter 23, Acute Coronary
Syndrome: ST Elevation Myocardial Infarction (see Fig.
23.26A,B). Because leads V7 to V9 are not routinely
recorded, ST depression confined to V1 to V3 can be mis-
taken for non-ST elevation MI or unstable angina.
Occlusion of the left main coronary artery: Total
occlusion of the left main coronary artery is usually fa-
tal and most patients do not survive to reach a medical
facility. Total or subtotal occlusion of the left main
coronary artery will show diffuse ST segment depres-
sion in multiple leads especially V4 to V6 and in leads I,
II, and aVL. Leads aVR and V1 show elevation of the ST
segments with ST elevation in aVR  ST elevation in
V1 (Fig. 24.18, arrows). Because these leads are not ad-
jacent to each other, thrombolytic therapy is not indi-
cur when there is severe triple vessel disease. These
ECG changes indicate extensive myocardial injury that
will require aggressive therapy including early coro-
nary revascularization.
Digitalis effect: The scooping type of ST depression,
as shown in Figure 24.19, is usually from digitalis effect.
Secondary ST segment depression: Secondary ST
depression from left ventricular hypertrophy with
strain pattern is shown in Figure 24.20.
Mechanism of ST Elevation and ST
Depression
Deviation of the ST segment as a result of myocardial
ischemia has been ascribed to two different mecha-
nisms namely systolic current of injury or diastolic
current of injury.
Systolic Current of Injury
ST elevation and ST depression from systolic
current of injury: When the myocardial cells are

Figure 24.17: ST Segment

Depression in the Anterior Pre-
cordial Leads. The ST depression
in the anterior precordial leads may
represent anterior subendocardial in-
jury, although this may also
represent a true ST elevation myocar-
dial infarction involving the left ven-
tricle posterolaterally.
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina 387

Figure 24.18: ST Depression from Subtotal Occlusion of the Left Main

Coronary Artery. Twelve-lead electrocardiogram (ECG) shows atrial fibrillation and
marked ST depression in multiple leads including V3 to V6 and leads I, II, aVL, and aVF. There is
also elevation of the ST segment in leads V1 and aVR. The ST elevation in aVR is higher than
the ST elevation in V1 (arrows). This type of ECG is frequently associated with subtotal occlu-
sion of the left main coronary artery or its equivalent.

A Figure 24.19: ST Segment De-

pression from Digitalis. (A) The
ST depression in leads II and V6
(arrows) has a scooping or slow
downsloping pattern. This type of
ST depression is due to digitalis.
(B) Leads II and V6 are magnified to
show the ST depression.

Lead II Lead V6
B

Figure 24.20: Left Ventricular Hypertrophy: Twelve-lead electrocardiogram show-

ing left ventricular hypertrophy (LVH) with downsloping ST depression from left ventricular
strain. The J point is not depressed and the ST segments have a downsloping configuration
with upward convexity (arrows). This type of LVH is usually seen in patients with
hypertension and is often described as pressure or systolic overload.
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388 Chapter 24

ST elevation due to systolic current of injury

Normal Systolic Current
Onset of Injury Myocardium
of injury
1 2
Injured
3 myocardium
0
-60 Mv
4 -90 Mv

After transmural Injury

Action Potential
ST Elevation
Onset of Injury

ECG

Figure 24.21: Systolic Current of Injury. The upper row represents transmembrane
action potentials before and after myocardial injury and the lower row the corresponding elec-
trocardiogram (ECG). A change in resting potential from 90 to approximately 60 mV will occur
when cells are injured. A less negative resting potential causes the amplitude and duration of the
action potential to diminish when compared to normal cells. This difference in potential creates
a current of injury during electrical systole (corresponding to phases 13 of the action potential
equivalent to the ST segment and T wave in the ECG) between normal and injured myocardium.
This current flows from normal myocardium toward the injured myocardium.Thus, if the injury is
subepicardial or transmural, the current of injury is directed toward the overlying electrode
resulting in ST elevation. (0 to 4 represent the different phases of the action potential.)

ST elevation due to diastolic current of injury

Phase 4 becomes
less negative Diastolic
1 2
Current of
Injury Previous
0 3 Baseline
-60 Mv 4
4 -90 Mv

Action Potential Onset of Injury After transmural Injury

ECG baseline (T-Q segment) Previous Baseline

shifted downward Apparent ST
Elevation

ECG Onset of Injury

T-Q segment

Figure 24.22: Diastolic Current of Injury. The yellow shaded areas in the upper and lower
diagrams represent electrical diastole showing a change in resting potential from 90 to 60 mV
after myocardial injury. Because the resting potential of injured cells is less negative, the cells are
relatively in a state of partial depolarization.Thus, the extracellular membrane of the injured cells
is more negative (less positive) compared with that of normal myocardium causing a diastolic
current of injury directed away from the injured myocardium. This diastolic current of injury
causes the TQ segment to be displaced downward away from the overlying electrode. When all
cells are discharged during systole, the potential gradient between injured and normal cells is di-
minished, shifting the electrocardiogram baseline to its original position, resulting in apparent ST
elevation.
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina 389

ST depression due to diastolic current of injury Figure 24.23: ST Segment

Endocardial Cells
Depression. When there is
Diastolic Epicardial Cells
1 2 Phase 4 less Phase 4 more subendocardial injury, the ST seg-
negative Current of
negative ment is depressed because the
Injury
0 3
baseline is shifted upward away
-60 Mv 4 from the injured subendocardium
4 -90 Mv
toward the direction of the
Onset of Injury After subendocardial Injury recording electrode. See text.
Action Potential
Previous
Apparent ST Baseline
Depression

Onset of Injury will shift baseline

ECG baseline (T-Q segment)
away from subendocardium
ECG toward the electrode
shifted upward

injured, the resting potential of injured cells is less neg-
ative compared with normal cells. A less negative resting
potential will diminish the height, amplitude, and dura-
tion of the action potential (Fig. 24.21). This difference
in the action potential between normal cells and injured
cells creates a current of injury during electrical systole
(phases 13 or ST segment and T wave in the ECG) that
is directed toward the injured myocardium. Thus, if the
injury is transmural or subepicardial, the injury current
is directed subepicardially resulting in elevation of the
ST segment in the recording ECG electrodes that overlie
the area of injury (Fig. 24.21). If the injury is confined to
the subendocardium, the current of injury is directed
subendocardially, away from the recording electrodes,
resulting in depression of the ST segment.
Diastolic Current of Injury
Apparent ST segment elevation from diastolic
current of injury: The resting potential of injured my-
ocardial cells is less negative compared with normal
cells. This difference in potential occurs during phase
4, which corresponds to the TQ segment in the ECG.
Because the injured cells have a less negative resting po-
tential, they will have a more negative (less positive) ex-
tracellular charge relative to normal myocardium. This
difference in potential between normal and injured
myocardium will create an electrical gradient during
diastole that is directed away from the injured cells, to-
ward the more positive normal myocardium. This
causes the ECG baseline (TQ segment) to shift down-
ward, away from the surface electrode overlying the
area of injury (Fig. 24.22). During systole, all myocar-
dial cells are discharged, erasing the potential differ-
ence between injured cells and normal cells. This will
cause the ECG to compensate and return the ST seg-
ment to its previous baseline before the injury, result-
ing in apparent ST elevation. The opposite will occur if
the injury is subendocardial.
Apparent ST segment depression from diastolic
current of injury: The mechanism of ST segment de-
pression from subendocardial injury is shown in Figure
24.23. When there is subendocardial injury, phase
4 or resting potential of the injured subendocardial

Zone of ischemia

Zone of injury

Depolarization

Zone of necrosis

Figure 24.24: Q Waves. Diagrammatic representation of a transmural infarct. The

necrotic area (black) involves the whole thickness of the myocardium and consists of
cells that cannot be depolarized. Thus, an electrode overlying the necrotic area will
normally record the electrical activity on the opposite side of the myocardium (red arrow),
resulting in q waves.
LWBK271-C24_379-395.qxd 1/29/09 1:56 PM Page 390 LWBK271-C01_01-08.qxd
390 Chapter 24
myocardial cells is less negative when compared with
normal myocardial cells. This difference in potential be-
tween normal and injured myocardium will create an
electrical gradient during diastole. Because the injured
cells are in a state of partial depolarization, a diastolic
current of injury is directed away from the injured suben-
docardium toward the normal subepicardium causing
the TQ segment to shift upward toward the surface elec-
trode overlying the ischemic area. During systole, all my-
ocardial cells are discharged simultaneously, erasing the
diastolic gradient between injured cells and normal cells.
This will cause the ECG to compensate and return the
ST segment to its previous baseline before the injury, re-
sulting in apparent ST segment depression (Fig. 24.23).
In summary, the direction of systolic current of injury
is always toward the injured myocardium, whereas di-
astolic current of injury, equivalent to the TQ segment,
is always directed away from the injured myocardium.
Q Waves
Pathologic Q waves: Pathologic Q waves can be pre-
vented if the ischemic process is relieved within a timely
fashion. However, if myocardial injury progresses, my-
ocardial necrosis will occur resulting in pathologic Q
waves. Electrocardiographically, Q waves indicate trans-
mural myocardial necrosis, which signify permanent
myocardial damage and are usually not reversible.
However, some Q waves may reverse because of con-
traction of the scar tissue during the healing process.
Additionally, the injured myocardium may be tem-
porarily stunned during the acute episode and may be
unable to conduct an electrical impulse locally, which
may be transient and reversible. Pathologic Q waves is
the usual sequelae of ST elevation MI, although it may
also occur in approximately 25% of patients with non-
ST elevation MI. Abnormal Q waves have been previ-
ously discussed in Chapter 23, Acute Coronary Syn-
drome: ST Elevation Myocardial Infarction.
Summary of the evolution of the ECG in acute
coronary syndrome:
T-wave abnormalities: Alterations confined to the
T waves indicate myocardial ischemia. These T-wave
abnormalities are reversible. However, if the is-
chemic process continues unabated, alterations in
the ST segment will follow.
ST segment abnormalities: Changes involving
the ST segment suggest a more advance stage of my-
ocardial ischemia and indicate myocardial injury.
Alterations involving the ST segment and T wave
may be reversible. However, if the ischemic process
continues unrelieved, changes in the QRS complex
will follow.
Q waves: Q waves indicate the presence of myocar-
dial necrosis and are usually not reversible.
Non-ST Elevation MI and
Unstable Angina
ECG of Non-ST Elevation MI and
Unstable Angina
1. J point and ST segment depression of 1 mm below baseline.
2. Symmetrically inverted T waves measuring 2 mm.
3. The ST and T wave abnormalities may be less specific.
Mechanism
Normal ventricular myocardium: Unlike the single muscle
cell where depolarization and repolarization occur in the
same direction, depolarization and repolarization of the nor-
mal ventricular myocardium occur in opposite directions.
Thus, depolarization of the myocardium is endocardial to
epicardial because the impulse originates from the Purkinje
fibers, which are located subendocardially. An electrode
overlying the myocardium will record a tall QRS complex.
Although the epicardium is the last to be depolarized, it is the
earliest to recover because it has shorter action potential du-
ration compared to other cells in the myocardium. Thus, the
repolarization wave travels from epicardium to endo-
cardium, away from the recording electrode resulting in up-
right T wave in the ECG. In addition to the shorter action po-
tential duration of epicardial cells, there are other reasons
why the epicardium recovers earlier than the endocardium,
even if the epicardium is the last to be depolarized.
The subendocardium has a higher rate of metabolism,
thus requiring more oxygen when compared with the epi-
cardium.
The subendocardium is the deepest portion of the my-
ocardium and is farthest from the coronary circulation.
The subendocardium is immediately adjacent to the ven-
tricular cavities. Because the ventricles generate the highest
pressure in the cardiovascular system, the subendocardium
is subject to a higher tension than the epicardium.
Repolarization (the ST segment and T wave) occurs dur-
ing systole when the myocardium is mechanically con-
tracting. There is no significant myocardial perfusion
during systole especially in the subendocardium at the
time of repolarization.
Myocardial ischemia: Myocardial ischemia is a pathologic
condition resulting from an imbalance between oxygen sup-
ply and demand. Depending on the severity of myocardial is-
chemia, the ECG changes may involve the T wave, the ST seg-
ment, or the QRS complex. Changes confined to the T waves
are traditionally called myocardial ischemia. Alterations in
the ST segment are described as myocardial injury and when
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina
the QRS complex is altered with development of pathologic
Q waves or decreased amplitude of the R wave, the abnor-
mality is myocardial necrosis.
Changes involving the T waves: Changes affecting only
the T waves indicate myocardial ischemia, which may be
subendocardial resulting in tall T waves or transmural re-
sulting in deeply inverted T waves. An abnormal T wave
associated with troponin elevation is consistent with non-
ST elevation MI or more specifically, a T-wave infarct.
n Subendocardial ischemia: The endocardial cells im-
mediately adjacent to the ventricular cavities are able
to extract nutrients directly from blood within the ven-
tricles. Thus, it is the deeper subendocardial cells and
not the endocardium itself that are at risk for myocar-
dial ischemia. When there is subendocardial ischemia,
the repolarization wave is not significantly altered and
normally starts from epicardium to endocardium re-
sulting in upright T waves. The repolarization wave,
however, is delayed after it reaches the ischemic area,
causing the T wave to be symmetrical and taller than
normal in leads overlying the area of ischemia.
n Transmural or subepicardial ischemia: If the ischemia
is transmural involving the whole thickness of the my-
ocardium, the direction of the repolarization wave is
reversed, starting from endocardium to epicardium,
causing the T wave to become deeply inverted instead
of upright. Because the duration of the action potential
of ischemic cells becomes longer than normal, the re-
polarization wave travels slowly causing the T wave to
be symmetrical with slightly prolonged QT.
Changes involving the ST segment: Changes in the ST
segment indicate myocardial injury, which is a more ad-
vanced form of myocardial ischemia. Myocardial injury
may be transmural resulting in ST segment elevation or it
may be subendocardial, resulting in ST segment depression.
n Transmural or subepicardial injury: Transmural or
subepicardial injury causes the ST segment to become
elevated. ST elevation is a more severe form of my-
ocardial injury, which is almost always associated with
troponin elevation consistent with ST elevation MI.
Elevation of the ST segment may be due to systolic or
diastolic current of injury.
n Systolic current of injury: Systolic current of in-
jury occurs during phases 1 through 3 of the action
potential corresponding to the ST segment and T
wave in the ECG. Systolic current of injury always
points to the direction of the injured myocardium.
This causes the ST segment to become elevated in
leads overlying the area of injury.
n Diastolic current of injury: Diastolic current of
injury occurs during phase 4 of the action poten-
tial corresponding to the T-Q segment in the ECG.
Diastolic current of injury is always directed away
from the area of injury. Thus, the baseline or T-Q
segment of the ECG is shifted downward, away
391
from the recording surface electrode overlying the
area of injury. During electrical systole correspon-
ding to the QT interval in the ECG, all cells are de-
polarized, eliminating all the electrical charges of
both injured cells and normal cells. This will cause
the ECG to compensate and return the ST segment
back to its previous baseline before the injury, re-
sulting in apparent ST elevation. In pericarditis,
only the epicardial cells are injured. The endocardial
cells remain preserved. A diastolic current of injury
will flow from epicardium to endocardium, away
from the injured area and away from the recording
surface electrodes. This will similarly cause the base-
line T-Q segment to shift downward. During electri-
cal systole, apparent ST segment elevation will occur
as the ECG returns to its previous baseline.
n Subendocardial injury: Subendocardial injury de-
presses the ST segment and represents a less severe
form of myocardial injury involving the subendo-
cardium. ST depression with troponin elevation is
non-ST elevation MI. More specifically, it is an ST de-
pression MI. Depression of the ST segment may be
due to systolic or diastolic current of injury.
n Systolic current of injury: Systolic current of injury
always flows toward the area of injury. Thus, a current
of injury flows from normal myocardium (subepi-
cardium) toward the subendocardium, away from
the recording surface electrode, resulting in depres-
sion of the ST segment.
n Diastolic current of injury: Diastolic current of in-
jury flows in the opposite direction, which is away
from the injured myocardium. Thus, during electri-
cal diastole, the current of injury will flow away
from subendocardium toward normal myocardium
(subepicardium) in the direction of the recording
electrode, shifting the T-Q segment upward. During
electrical systole, all cells are discharged, eliminat-
ing the potential difference between injured cells
and normal cells. This will cause the ECG to com-
pensate and return the ST segment downward to
its previous baseline before the injury, resulting in
apparent ST depression.
Changes involving the QRS complex: If myocardial is-
chemia is not relieved and collateral flow is not adequate,
myocardial injury will progress irreversibly to myocardial
necrosis resulting in alteration of the QRS complex. Thus,
changes in the QRS complex resulting in pathologic Q
waves or diminished amplitude of the R wave represent
transmural myocardial necrosis. These changes are usu-
ally permanent. Cells that are necrotic or infarcted do not
depolarize or conduct electrical activity. If an electrode is
positioned over a necrotic myocardium, Q waves or QS
complexes will be recorded, which represent activation of
normal myocardium away and opposite the infarcted
area, causing a negative deflection in the ECG.
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392 Chapter 24
Clinical Implications
Myocardial ischemia with elevation of the ST segment is due
to complete occlusion of the vessel lumen. When blood sup-
ply is completely interrupted for a duration of more than 20
minutes, myocardial necrosis always occurs and troponin el-
evation is always expected.
Myocardial ischemia with depression of the ST segment or
inversion of the T wave may be due to either diminished
coronary flow or increased myocardial oxygen demand or a
combination of both. It may also be due to a completely oc-
cluded artery, but has collateral flow. These ST and T wave
Treatment
abnormalities may or may not be associated with troponin
elevation, depending on the severity of myocardial ischemia.
When cardiac troponins are elevated in the circulation, non-
ST elevation MI is present. If the troponins are not elevated,
the clinical picture is one of unstable angina. These patients
with non-ST elevation MI or unstable angina may not show
any abnormalities in the ECG.
Unlike ST segment elevation and pathologic Q waves,
T-wave inversion is not specific for myocardial ischemia.
Although deep and symmetrical T-wave inversions measur-
ing 2 mm are typical for myocardial ischemia, ischemic-
looking T waves may be seen in patients without ischemic
heart disease.
ST depression from myocardial injury usually measures 1
mm. The ST depression may be horizontal, downsloping, or
slow upsloping in configuration. The J point (junction be-
tween the QRS complex and ST segment) should be de-
pressed by 1 mm if the ST depression is from myocardial
ischemia. ST depression is less specific if the J point is not de-
pressed or if the J point is depressed by 0.5 mm. ST depres-
sion is not only the result of myocardial ischemia, but could
also be due to the effect of drugs such as digitalis, antiar-
rhythmic agents, Ritalin, and tricyclic antidepressants. ST de-
pression can also occur in patients with cardiac diseases not
due to ischemia such as left ventricular hypertrophy, elec-
trolyte abnormalities, mitral valve prolapse, and other non-
cardiac abnormalities, including anemia.
The severity of ST depression and T wave inversion provide
important diagnostic and prognostic information. For ex-
ample, patients with ST depression 0.5 mm have higher
morbidity and mortality compared to patients with T wave
inversion or those without ECG findings.
Although ST elevation MI is synonymous with a Q wave MI,
not all patients with ST elevation will develop Q waves. Ad-
ditionally, approximately 25% of patients with non-ST eleva-
tion MI will also develop Q waves. The rest (75%) will have a
non-Q wave MI. Thus, ST elevation MI and non-ST eleva-
tion MI are preferred over Q wave and non-Q wave MI. Sim-
ilarly, Hurst emphasizes that non-ST elevation MI, which is
the terminology used in the American College of Cardiology/
American Heart Association (ACC/AHA) guidelines, does
not specify the abnormality present in the ECG. Thus, when
a non-ST elevation MI occurs, he prefers to identify the
infarct either as a T-wave MI or ST depression MI rather
than a non-ST elevation MI.
The infarct related artery can be predicted using the 12-lead
ECG when there is ST elevation MI, T-wave MI, or Q-wave
MI. Identifying the culprit vessel is more difficult when the
MI is associated with ST segment depression. Very often, my-
ocardial ischemia with ST segment depression is due to mul-
tivessel coronary disease, including the possibility of a signif-
icant left main coronary artery lesion.
Unlike ST elevation MI, which indicates that the coronary ar-
tery is completely occluded and there is urgency in immedi-
ately establishing coronary flow with a thrombolytic agent or
primary PCI, non-ST elevation MI and unstable angina indi-
cate that the coronary artery is partially occluded, resulting
in imbalance between oxygen supply and demand. Thus, the
patient can be initially risk stratified so that patients who are
high risk for reinfarction or death should undergo an early
invasive strategy, whereas patients who are not identified as
being high risk can undergo an early conservative approach.
Early conservative: The early conservative approach in-
cludes mainly medical therapy. Cardiac catheterization is
reserved only when there is evidence of continuing is-
chemia either spontaneously occurring or exercise in-
duced in spite of intensive medical therapy.
Early invasive: The early aggressive approach includes
medical therapy and an early invasive strategy with car-
diac catheterization and revascularization of the occluded
vessel performed within 4 to 24 hours after the patient is
hospitalized regardless of the presence or absence of con-
tinuing ischemia.
High-risk patients: According to the ACC/AHA 2007
guidelines for the management of patients with unstable
angina and non-ST elevation MI, high-risk patients include
any of the following findings:
Recurrent angina or ischemia at rest or with low-level ac-
tivities despite intensive medical therapy
Elevated cardiac biomarkers
New or presumably new ST depression
Signs or symptoms of heart failure or new or worsening
mitral regurgitation
High-risk findings from noninvasive testing
Hemodynamically unstable patient
Sustained ventricular tachycardia
Left ventricular dysfunction with ejection fraction of
40%
Previous PCI within 6 months
Prior coronary artery bypass surgery
High risk score using risk stratification models
Antiplatelet and anticoagulant therapy: Antithrombotic
agents are the mainstay in the therapy of patients with non-ST
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Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina 393

TABLE 24.1

Summary of the Initial and Maintenance Doses of Aspirin and Clopidogrel according to the American
College of Cardiology/American Hospital Association 2007 Guidelines on Non-ST Elevation
Myocardial Infarction and Unstable Angina
Percutaneous Coronary Intervention
Medically Treated
(No Stent) Bare Metal Stent Sirolimus Stent Paclitaxel Stent
Aspirin (initial dose) 162325 mg 162325 mg 162325 mg 162325 mg
Minimum duration 162325 mg for 162325 mg for 162325 mg for
1 month 3 months 6 months
Maintenance dose 75162 mg daily 75162 mg daily 75162 mg daily 75162 mg daily
indefinitely indefinitely indefinitely indefinitely
Clopidogrel 300600 mg 300600 mg 300600 mg 300600 mg loading
(initial dose) loading dose loading dose loading dose dose
Minimum duration 75 mg daily for 75 mg daily for 75 mg daily for 75 mg daily for
1 month 1 month 12 months 12 months
Maintenance dose Ideally up to Ideally up to Ideally up to Ideally up to 12 months
12 months 12 months 12 months

elevation MI and unstable angina, whether or not an early
conservative or a more aggressive strategy is used.
Aspirin: Aspirin should be given as soon as possible, often
in the prehospital setting when diagnosis of acute coronary
syndrome is suspected. The initial dose of aspirin is 162 to
325 mg of plain (nonenteric coated) aspirin given orally.
n Medically treated patients: Among patients who are
treated medically and are not stented, aspirin is con-
tinued at a dose of 75 to 162 mg daily indefinitely.
n Stented patients: In patients undergoing PCI with
stent placement, the dose of enteric-coated aspirin de-
pends on the type of stent used.
n Bare metal stent: Aspirin is given at a dose of 162 to
325 mg daily given for at least 1 month if a bare metal
stent was deployed. This is followed by 75 to 162 mg
daily indefinitely.
n Drug-eluting stent: The dose of aspirin is 162 to 325 mg
daily for at least 3 months if a sirolimus-coated stent
was deployed and for at least 6 months for paclitaxel-
coated stent. This is followed by a maintenance dose
of 75 to 162 mg daily indefinitely.
Clopidogrel: The loading dose of clopidogrel is usually
300 mg given orally. A higher loading dose of 600 to 900
mg inhibits platelets more rapidly, although its safety and
clinical efficacy needs to be established.
n Medically treated patients: Among medically treated
patients who are not stented, 75 mg of clopidogrel is
given daily for at least 1 month and ideally up to
1 year. Clopidogrel should not be given or should be
discontinued for 5 to 7 days in patients undergoing
coronary bypass surgery.
n Bare metal stent: Clopidogrel is given at a maintenance
dose of 75 mg/day for at least 1 month and ideally up to
1 year for patients who have bare metal stents.
n Drug-eluting stent: The maintenance dose is 75 mg
daily for at least 1 year.
Table 24.1 summarizes the initial dose, minimum dura-
tion, and maintenance dose of aspirin and clopidogrel ac-
cording to the ACC/AHA 2007 guidelines on non-ST ele-
vation MI and unstable angina.
Unfractionated heparin or low-molecular-weight
heparin
n Patients undergoing PCI: Intravenous unfractionated
heparin or subcutaneous low-molecular-weight he-
parin in addition to aspirin and clopidogrel is a
Class I recommendation in patients undergoing
PCI. Enoxaparin, a low-molecular-weight heparin, is
preferred to unfractionated heparin except when there
is renal failure or when bypass surgery is planned
within 24 hours. The use of bivalirudin or fonda-
parinux also receives a Class I recommendation.
n Patients not undergoing PCI: The use of unfraction-
ated heparin, enoxaparin, and fondaparinux among
patients who are treated conservatively also receives a
Class I recommendation. Fondaparinux is the pre-
ferred agent when there is increased risk of bleeding.
Enoxaparin and fondaparinux is preferred over un-
fractionated heparin unless bypass surgery is being
planned within 24 hours.
IIb/IIIa antagonists:
n Patients undergoing PCI: The use of IIb/IIIa platelet
antagonists such as abciximab (ReoPro), eptifibatide
LWBK271-C24_379-395.qxd 1/29/09 1:56 PM Page 394 LWBK271-C01_01-08.qxd
394 Chapter 24
(Integrilin), or tirofiban (Aggrastat) is a Class I indica-
tion for patients with acute coronary syndrome un-
dergoing PCI.
n Patients not undergoing PCI: For patients not under-
going PCI, IIb/IIIa antagonists can also be given as
medical therapy to high-risk patients in addition to
aspirin and clopidogrel. Patients appear to benefit
with tirofiban or eptifibatide (Class IIb recommenda-
tion), but not with abciximab. The use of abciximab,
therefore, as medical treatment of acute coronary syn-
drome in patients who are not undergoing PCI is not
recommended (Class III).
Thrombolytic agents: Thrombolytic agents such as al-
teplase, streptokinase, reteplase, or tenecteplase are con-
traindicated in non-ST elevation MI and unstable angina.
In addition to the use of antiplatelet agents, the general med-
ical therapy of non-ST elevation MI and unstable angina is
similar to that of ST elevation MI because both entities have
the same pathophysiologic substrate: plaque rupture with
thrombotic occlusion of the vessel lumen. General medical
therapy for patients with non-ST elevation MI and unstable
angina are similar and include:
Oxygen: Oxygen is initially given to patients with hypox-
emia or arterial oxygen saturation of 90% or those of
questionable respiratory status.
Nitroglycerin: Nitroglycerin 0.4 mg sublingual tablets or
spray 5 minutes apart for 3 doses followed IV if there are
symptoms of ischemia. The IV infusion is started at 10
mcg/minute and increased by 10 mcg/minute every 3 to 5
minutes until symptoms are improved or systolic blood
pressure drops. No definite maximum dose is recom-
mended although the top dose is usually 200 mcg/minute.
Morphine: Morphine sulfate 1 to 5 mg IV may be given if
chest pain is not relieved after three sublingual nitroglyc-
erin tablets or chest pain recurs in spite of anti-ischemic
therapy. This may be repeated every 5 to 30 minutes if
necessary. Although morphine sulfate continues to be a
Class I indication for patients with ST elevation MI, the
more recent ACC/AHA 2007 guidelines on non-ST eleva-
tion MI has downgraded the use of morphine for is-
chemic pain associated with non-ST elevation MI and
unstable angina from Class I to Class IIa.
Beta blockers: The latest 2007 AHA/ACC guidelines rec-
ommend that beta blockers should be given orally within the
first 24 hours when there are no contraindications. Con-
traindications to beta blocker therapy include PR interval
0.24 seconds, second degree atrioventricular block or
higher, severe left ventricular dysfunction, or history of
asthma. The agent should be gradually titrated in patients
with moderate left ventricular dysfunction. Intravenous beta
blockers should be used cautiously and avoided when there
is heart failure, hypotension, or hemodynamic instability.
Renin-angiotensin antagonists: Angiotensin-convert-
ing enzyme inhibitors or angiotensin receptor blockers
and aldosterone antagonists should be given when there is
associated left ventricular dysfunction in the absence of
contraindications.
Statins: Statins to lower the low-density lipoprotein to a
target goal of 70 mg/dL.
Patients who continue to have ischemia, the following agents
or procedures can be given:
A combination of nitrates and beta blockers are the drugs
of choice for myocardial ischemia.
Calcium blockers are second- or third-line agents:
n Calcium channel blockers may be given if ischemia is
not relieved by nitrates and beta blockers.
n Nondihydropyridine calcium antagonists such as ver-
apamil and diltiazem are given when beta blockers are
contraindicated.
n Calcium channel blockers should not be given when
there is evidence of left ventricular dysfunction.
n Intra-aortic balloon pump may be used for severe is-
chemia not responsive to medical therapy.
n Oxygen and morphine sulfate is usually given as part
of general medical therapy
Prognosis
Non-ST elevation MI and unstable angina have a lower in-
hospital mortality of approximately 1% to 3% when com-
pared with ST elevation MI. Myocardial involvement is less
extensive and left ventricular systolic function is usually pre-
served.
Non-ST elevation MI is associated with a higher recurrence
of cardiovascular events after hospital discharge compared
with ST elevation MI and exacts a higher post-hospital mor-
tality. Although ST elevation MI has a higher initial mortal-
ity, overall mortality of ST and non-ST elevation MI will be
similar after a 2- to 3-year follow-up. Patients with non-ST
elevation MI and unstable angina who are high risk for car-
diovascular events should be identified so that they can be
revascularized.
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Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guide-
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25
Electrolyte Abnormalities
Hyperkalemia
Among the various electrolyte abnormalities, hyper-
kalemia, hypokalemia, hypercalcemia, and hypocal-
cemia are the only disorders that can cause reliable di-
agnostic changes in the electrocardiogram (ECG).
These ECG changes can be recognized well before the
results of the laboratory tests become available. The
severity of these electrolyte abnormalities usually par-
allels the changes in the ECG.
A simple rule to remember regarding the effect of
these electrolyte abnormalities on the ECG is that
when increased levels are present (hyperkalemia or
hypercalcemia), the QT interval is shortened. In-
versely, when decreased levels of these electrolytes
are present (hypokalemia or hypocalcemia), the QT
interval is prolonged. Figure 25.1 shows the ECG ab-
normalities associated with each of these electrolyte
disorders.
The normal level of serum potassium varies from 3.3 to
5.3 millimoles per liter (mmol/L), also expressed as
milliequivalents per liter (mEq/L). Hyperkalemia im-
Figure 25.1: Electrolyte Abnormalities. Only dis-
orders of potassium and calcium can be reliably
diagnosed in the electrocardiogram. When the serum
level of these electrolytes is increased (hyperkalemia and
hypercalcemia), the QT interval is shortened, whereas
when the serum level is low (hypokalemia and hypocal-
cemia), the QT interval is prolonged.
Normal
396
plies the presence of higher than normal levels of
serum potassium.
Among the electrolyte disorders, hyperkalemia is the
most fatal. It also exhibits the most remarkable
changes in the ECG. The ECG abnormalities gener-
ally reflect the increasing severity of the hyper-
kalemia, thus the ECG is useful not only in the diag-
nosis of this electrolyte disorder, but is also helpful in
determining the intensity in which hyperkalemia
should be treated.
Figure 25.2 is a diagrammatic representation of the
ECG changes associated with increasing levels of potas-
sium in the serum.
Mild hyperkalemia (6.0 mmol/L): Peaking of
the T waves occurs and may be the earliest and only
abnormality that can be recognized. The QT inter-
val is normal or shortened (Fig. 25.2B).
Moderate hyperkalemia (6.0 to 7.0 mmol/L):
More pronounced peaking of the T waves occur,
QRS complexes widen, P waves become broader
with diminished amplitude, and PR interval
lengthens resulting in atrioventricular (AV) block
(Fig. 25.2C).
Hypercalcemia Hypocalcemia
Hyperkalemia Hypokalemia
Short QT Prolonged QT
LWBK271-C25_396-413.qxd 29/1/09 7:20 pm Page 397 LWBK270-4119G-C02_073-110.qxd
A B
Figure 25.2: The Electrocardiogram of Hyperkalemia. Diagram depicts the electrocar-
diogram changes as the level of hyperkalemia increases. (A) Normal, (B) mild to moderate hyper-
kalemia, (C) moderate, and (D) severe hyperkalemia.
Severe hyperkalemia (7.0 mmol/L): P waves
become unrecognizable, further widening of the
QRS complex occurs, S and T waves merge with a
very short ST segment resulting in a sinusoidal
wave, ST segment may be elevated in V12 and mis-
taken for acute ischemic injury, and, finally, slowing
of the heart rate, asystole, or ventricular flutter can
occur (Fig. 25.2D).
Mild hyperkalemia (6.0 mmol/L): Peaking of
the T waves is the earliest to occur and is the most
characteristic ECG pattern of hyperkalemia. Hyper-
kalemic T waves are often described as tented be-
cause they closely resemble the shape of a tent. The T
waves are tall and symmetrical with a pointed tip
and a narrow base (Fig. 25.325.5). The QT interval
is generally short, unless coexisting abnormalities
such as hypocalcemia or myocardial disease are
present.
Moderate hyperkalemia (6.0 to 7.0 mmol/L): As
the level of serum potassium increases, the amplitude
of the T wave also increases and often the height of the
RR = 0.86 sec
QT = 0.34 sec
Figure 25.3: TentedT waves. The most distinctive
abnormality in hyperkalemia is the presence of tented T waves
characterized by tall, peaked, and symmetrical T waves with a
narrow base and short QT interval. In the above example, the QT
interval measures 0.34 seconds.
Electrolyte Abnormalities 397
C D
T wave becomes taller than the R wave. The T waves are
tallest in precordial leads V24, because of the proximity
of these leads to the myocardium (Figs. 25.525.7).
The onset of the P wave and QRS abnormalities is
more difficult to predict than the T wave changes. In
general, the P waves and QRS complexes start to
widen when moderate hyperkalemia is present, as
conduction through the atria and ventricles becomes
delayed (Fig. 25.7).
Severe hyperkalemia (7.0 mmol/L): When the
potassium level increases to 7.0 mmol/L, the ampli-
tude of the P wave decreases until the P waves are no
longer detectable. The absence of P waves in spite of
normal sinus rhythm is due to marked slowing of the
sinus impulse across the atria or the sinus impulse
traveling through specialized internodal pathways.
Sinoventricular rhythm is the term used to describe
sinus rhythm without any discernible P waves.
Sinoventricular rhythm is impossible to distinguish
from junctional rhythm when the QRS complexes are
narrow or from accelerated ventricular rhythm when
the QRS complexes are wide.
Other ECG changes associated with severe hyper-
kalemia are shown in Figs. 25.7 through 25.15:
Further widening of the QRS complex, shortening
of the ST segment and fusion of the S wave with the
T wave resembling a sine wave (Figs. 25.7, 25.12, and
25.13).
P waves completely disappear in spite of the rhythm
being normal sinus, resulting in sinoventricular
rhythm (Figs. 25.8, 25.1025.15).
ST segment elevation mimicking acute ischemic in-
jury can occur, especially in the right sided precor-
dial leads V12 (Fig. 25.9).
Severe bradycardia (Figs. 25.1025.15) or ventricu-
lar flutter/fibrillation may occur.
Figures 25.11 through 25.13 are from the same patient
showing increasing levels of potassium.
Figures 25.14 and 25.15 show very high potassium lev-
els, which can lead to cardiac arrest.
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398 Chapter 25

Figure 25.4: Mild Hyperkalemia. The most significant electrocardiogram finding of mild hyperkalemia is the
presence of peaked T waves in virtually all leads with upright T waves as shown.

Figure 25.5: Moderate Hyperkalemia. Potassium level is 6.6 mmol/L. Peaking of the T waves (arrows) is
noted diffusely.The T waves are tented with a pointed tip and a narrow base. The T waves measure 10 mm in V3 and
are taller than the QRS complexes.

A. Before therapy (V1-V6) B. After therapy (V1-V6)

Figure 25.6: Wide QRS Complex. (A) Before therapy, the potassium level is 6.6 mmol/L.The QRS complexes in
the precordial leads are wide measuring 124 milliseconds.The R waves are upright in V1 (arrows). (B) Posttherapy,
potassium level is 4.6 mmol/L. The QRS complexes are narrower and the tall R waves in V1 are no longer present
(arrows). ms, milliseconds.
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Electrolyte Abnormalities 399

Figure 25.7: Severe Hyperkalemia with Widening of the QRS Complexes. Potassium level is 7.6
mmol/L. The PR interval is slightly prolonged. The QRS complexes are wide with marked peaking of the T waves.The
S wave continues directly into the T wave in leads II, aVF, and V2 to V5, resembling a sine wave.

Figure 25.8: Marked Bradycardia in a Patient with Severe Hyperkalemia. Potassium level is
8.3 mmol/L. The QRS complexes are widened and are not preceded by P waves. There is marked peaking of the T
waves, which is the hallmark of hyperkalemia. The rhythm is often called junctional, but is impossible to differenti-
ate from sinoventricular rhythm, which is sinus rhythm without discernible P waves.

Figure 25.9:Severe Hyperkalemia with ST Elevation in V1V2 Resembling Acute ST Elevation

Myocardial Infarction. Potassium level is 8.6 mmol/L. The T waves are markedly peaked in all leads especially V1
to V5, II, III, and aVF. The T wave in V3 measures almost 25 mm and most T waves are taller than the QRS complexes. ST
segment elevation in V12 can be mistaken for acute myocardial infarction or the ST elevation associated with the
Brugada electrocardiogram.
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400 Chapter 25

Figure 25.10: Absent P waves and Wide QRS Complexes in Severe Hyperkalemia. Potassium level is
9.0 mmol/L. P waves are absent and the QRS complexes are wide with a left bundle branch block configuration. The
rhythm is often called sinoventricular, although this is difficult to differentiate from accelerated idioventricular rhythm.

Figure 25.11: Generalized Peaking of the T Waves is the Hallmark of Hyperkalemia. Potassium level
is 8.7 mmol/L. In hyperkalemia, peaking of the T waves is generalized, occurring in almost all T waves that are
upright. Note that some of the T waves are taller than the QRS complexes.

Figure 25.12: The Presence of Sine Waves Indicate that the Hyperkalemia is Severe. Potassium level
is 8.9 mmol/L. Note that the sine waves are formed by the short ST segment causing the S waves to continue into
the T waves.These are seen in both limb and precordial leads.
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Electrolyte Abnormalities 401

Figure 25.13: Marked Widening of the QRS Complexes Indicates More Advanced Hyperkalemia.
Potassium level is 10.0 mmol/L.

ECG Findings of Hyperkalemia
1. Increased amplitude and peaking of the T waves. This is the
earliest, most consistent, and most characteristic ECG abnor-
mality associated with hyperkalemia. T-wave peaking persists
and worsens with increasing levels of hyperkalemia.
2. The QT interval is short or normal.
3. As hyperkalemia worsens, the QRS complexes widen.
4. The P wave becomes broader and the amplitude becomes
lower.
5. AV conduction becomes prolonged.
6. The P waves eventually disappear resulting in sinoventricular
rhythm.
7. The S wave continues into the T wave resulting in a sine wave
configuration.
8. Cardiac arrest from marked bradycardia, asystole, or ventricular
flutter/fibrillation.
Mechanism
The normal serum potassium varies from 3.3 to 5.3 mmol/L.
Hyperkalemia occurs when serum potassium exceeds 5.3
mmol/L. When extracellular potassium is increased, the ratio
between intracellular and extracellular potassium is decreased
and the resting membrane potential becomes less negative
(90 mV). This will affect the height and velocity of phase

Figure 25.14: Slow Ventricular Rhythm and Unusually Wide QRS Complexes. Potassium level is 10
mmol/L.The rhythm is unusually slow at 30 beats per minute with unusually wide QRS complexes with a left
bundle branch block pattern, peaked T waves, and no P waves. This rhythm usually precedes asystole or ventricular
fibrillation.
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402 Chapter 25

Figure 25.15: Marked Bradycardia with Wide Complexes, a Late Manifestation of Severe
Hyperkalemia. The initial potassium level is unknown. After the patient was resuscitated, the potassium level
was checked and found to be 8.8 mmol/L. The QRS complexes are wide with a very slow ventricular rate of 26 beats
per minute. No P waves can be identified. Peaking of the T waves persists in V2 and V3.

0 of the action potential. Slowing in conduction velocity in
the atria and ventricles will cause widening of the P wave and
QRS complex. As the severity of the hyperkalemia further in-
creases, the resting potential becomes less and less negative re-
sulting in further widening of the QRS complex and P wave.
Hyperkalemia also shortens phase 2, which is equivalent to
the plateau phase of the action potential. This will shorten the
ST segment in the ECG resulting in a shorter QT interval. It
also causes a more rapid phase 3 or steeper downslope of the
action potential resulting in peaking of the T waves.
Although the ECG findings may not consistently correlate
with the level of serum potassium, the following are the ECG
findings associated with increasing severity of hyperkalemia:
Mild hyperkalemia: 6.0 mmol/L
n Increased amplitude with peaking of the T waves is the
first abnormality to be detected when the potassium
level rises between 5 and 6 mmol/L. Hyperkalemic
T waves are typical and diagnostic in that the T waves
are tall and pointed with a narrow base and a normal
or short QT. The T waves become taller and more
peaked as the level of hyperkalemia progresses. The di-
agnosis of hyperkalemia is untenable unless the above
T-wave abnormalities are present. The T waves are
often taller than the R waves in precordial leads V2 to V4.
n The QT or corrected QT interval (QTc) is normal or
shortened. It is prolonged only when hyperkalemia is
associated with other electrolyte abnormalities such as
hypocalcemia or when there is associated myocardial
disease. This combination of hyperkalemia and hypo-
calcemia is commonly seen in patients with chronic
renal disease.
Moderate hyperkalemia: 6.0 to 7.0 mmol/L
n Widening of the P wave and QRS complex starts to
occur when the potassium level exceeds 6.0 mmol/L.
Widening of the QRS complex may be mistaken for
bundle branch block. Widening of the QRS complex
associated with hyperkalemia is reversible after the
electrolyte abnormality is corrected unlike preexistent
bundle branch block, which is persistent.
n Broadening of the P waves occurs when there is slowing
of conduction of the impulse across the atria. When the
P wave starts to widen, slight prolongation of the PR in-
terval and varying degrees of AV block may occur.
Severe Hyperkalemia: 7.0 mmol/L
n With increasing levels of serum potassium, further
widening of the QRS complex occurs accompanied by
shortening of the ST segment. The wide QRS complex
will eventually merge into the tall and peaked T wave
resembling a sine wave. The ST segments are often el-
evated in V12 and may be mistaken for acute ST ele-
vation myocardial infarction.
n Even when the rhythm remains normal sinus, the P
wave may not be evident in the ECG. The absence of P
waves in hyperkalemia even when the rhythm remains
normal sinus is called sinoventricular rhythm. The ab-
sence of P waves may be due to slow conduction of the
sinus impulse across the atria or the sinus impulse being
conducted through special internodal tracts between the
sinus node and AV node. Because the QRS complexes
are no longer preceded by P waves, the rhythm is impos-
sible to differentiate from AV junctional rhythm (when
the QRS complexes are narrow) or accelerated idioven-
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tricular rhythm (when the QRS complexes are wide).
Cardiac arrest may occur when the potassium level ex-
ceeds 8.5 mmol/L. This is preceded by marked slowing
of the heart rate, further widening of the QRS complexes,
asystole, or ventricular flutter/fibrillation.
Clinical Implications
Potassium is the major intracellular ion in the body. Approxi-
mately 98% of the total amount of potassium is intracellular
and the remaining 2% extracellular. This difference in concen-
tration between intracellular and extracellular potassium is
due to the presence of sodium potassium adenosine triphos-
phatase pump where 3 units of sodium is pumped out of the
cell in exchange for 2 units of potassium. The ratio between in-
tracellular and extracellular potassium makes the resting
membrane potential negative at approximately 90 mV.
Increased extracellular potassium may be due to increased
potassium load, worsening renal function, or acute shift of
intracellular potassium extracellularly. Increased potassium
in the diet by itself rarely causes hyperkalemia. Some drugs
can also cause hyperkalemia when there is renal dysfunction.
These include potassium supplements, potassium sparing di-
uretics (triamterene and amiloride), aldosterone antagonists
(spironolactone and eplerenone), angiotensin-converting
enzyme inhibitors, angiotensin receptor blockers, and non-
steroidal anti-inflammatory agents including the selective
cyclo-oxygenase 2 inhibitors. More commonly, hyperkalemia
is due to renal failure. It may also be the result of acute shift
of intracellular potassium to the extracellular space as when
cells are damaged from hemolysis or rhabdomyolysis. Acido-
sis can also cause a shift of H ions into the cell in exchange
for potassium that moves out of the cell. For every 0.1 unit
decrease in blood pH, the level of potassium in the serum in-
creases by approximately 0.5 mmol/L.
Among the electrolyte abnormalities, hyperkalemia causes
the most remarkable ECG abnormalities. The ECG changes
frequently parallel the severity of the electrolyte disorder.
The expected ECG findings, however, may not correlate well
with the potassium level because the effect of hyperkalemia
on the ECG depends on several factors and not just the
serum potassium level. These include the baseline level of
potassium, the rate of rise of potassium in the blood, coexist-
ing electrolyte abnormalities, coexisting metabolic abnor-
malities, and the presence or absence of myocardial disease.
Mild or moderate hyperkalemia is usually asymptomatic.
When significant hyperkalemia occurs usually 7.0 mmol/L,
symptoms include generalized weakness, paralysis, respiratory
failure from respiratory muscle weakness, and cardiac arrest.
Among all the electrolyte abnormalities, hyperkalemia is the
most fatal. Because severe hyperkalemia can be diagnosed in
the ECG, this will allow emergency treatment of the elec-
trolyte abnormality even before the results of the laboratory
become available.
Similarly, the ECG is useful in the diagnosis of pseudohyper-
kalemia. The laboratory may mistakenly report a high potas-
Electrolyte Abnormalities 403
sium level not the result of actual hyperkalemia but from he-
molysis after the blood is collected. If there are no associated
ECG changes, the diagnosis of hyperkalemia is unlikely. This
will obviate the need for unnecessary therapy.
Therapy
Treatment should be tailored according to the severity of the
hyperkalemia. The ECG abnormalities together with the
serum potassium level serve as useful guide in dictating the
intensity of management.
The American Heart Association (AHA) guidelines of car-
diopulmonary resuscitation and emergency cardiovascular care
recommend the following for the treatment of hyperkalemia.
Mild hyperkalemia, potassium level 6.0 mmol/L:
Potassium level 6.0 mmol/L is seldom of great concern.
The only therapy that may be needed is to identify the cause
of the hyperkalemia so that further increases in serum potas-
sium can be prevented. In addition, therapy may include re-
moval of potassium from the body.
Loop diuretics: Furosemide 40 to 80 mg IV or bumetanide
1 mg IV to enhance excretion of potassium.
Cation-exchange resin: Sodium polystyrene sulfonate
(Kayexalate) is given orally or by retention enema. The
oral dose can vary from 15 to 60 g daily. Fifteen grams is
given orally one to four times per day. Sorbitol 20%, 10 to
20 mL is given every 2 hours or as needed to prevent con-
stipation. Lower doses of Kayexalate of 5 to 10 g may be
given up to three times per day without laxative therapy. If
the patient is unable to take the resin orally, it can be given
as retention enema, 30 to 50 g every 6 hours in a warm
emulsion such as 50 mL 70% sorbitol mixed with 100 to
150 mL tap water and retained for at least 30 to 60 min-
utes. Each gram of Kayexalate removes approximately 1
mmol of potassium and takes at least 30 minutes to 2
hours to take effect. The resin binder carries a high sodium
load and should be given cautiously to patients in conges-
tive heart failure. The resin can also bind other cations
such as magnesium and calcium. These electrolytes should
be monitored together with the level of serum potassium.
Patients on digitalis should be monitored closely since hy-
pokalemia can aggravate digitalis toxicity.
Moderate hyperkalemia, potassium level 6.0 to 7.0
mmol/L: When moderate hyperkalemia is present, therapy
should be more emergent. In addition to eliminating the
cause of the hyperkalemia and removal of excess potassium
from the blood with loop diuretics and cation exchange
resins, the level of serum potassium can be lowered more
rapidly by shifting extracellular potassium intracellularly.
Glucose plus insulin: Twenty-five grams of glucose (50 mL
50% dextrose) is mixed with 10 units of regular insulin.
The solution is injected IV for over 15 to 30 minutes. Ten
units of regular insulin can also be mixed with 500 mL
10% glucose. The solution is given IV for 60 minutes. The
effect may last for 4 to 6 hours.
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404 Chapter 25
A B
Figure 25.16: The Electrocardiogram of Hypokalemia. (AD) Varying
levels of serum potassium. (A) Normal level of serum potassium. (B) Mild
hypokalemia. A prominent U wave is present. (C) Moderate hypokalemia.The U
wave becomes more prominent than the T wave. (D) Severe hypokalemia.There
is fusion of the T and U waves.
Sodium bicarbonate: 50 mEq is given IV over 5 min-
utes. Sodium bicarbonate lowers extracellular potassium
by shifting potassium into the cells. This agent is more ef-
fective when hyperkalemia is associated with metabolic
acidosis. The effect may last for 2 hours and may be re-
peated as necessary.
Nebulized albuterol: 10 to 20 mg nebulized over 15
minutes. B2 agonists shifts extracellular potassium intra-
cellularly and the effect may last for 2 hours. If insulin is
being given concomitantly, albuterol can attenuate its hy-
poglycemic effect.
Severe hyperkalemia and critical hyperkalemia, potas-
sium level 7.0 mmol/L: When serum potassium level ex-
ceeds 7.0 mmol/L or when the ECG abnormalities include
absent P waves and changes in the QRS, ST segment and T
waves, AV block or slowing of the heart rate, treatment of hy-
perkalemia should be very aggressive because severe hyper-
kalemia may cause lethal arrhythmias and cardiac arrest. The
following agents are given in order of priority according to
the AHA guidelines.
Calcium chloride: 10% 5 to 10 mL (500 to 1,000 mg) given
IV over 2 to 5 minutes. Calcium does not lower the level of
serum potassium but will stabilize myocardial membrane
against the toxic effects of potassium, thereby lowering the
risk of fatal arrhythmias including ventricular fibrillation.
The effect of calcium is immediate but lasts only for 20 to 40
minutes and repeated dosing may be needed.
Sodium bicarbonate: 50 mEq given IV over 5 minutes.
This should be injected using a separate tubing or IV line
from that used for calcium chloride.
Glucose plus insulin: Mix 10 units of regular insulin
with 50 mL 50% dextrose. The solution is given IV over
15 to 30 minutes.
Nebulized albuterol: 10 to 20 mg nebulized over 15
minutes.
Loop diuretics: as above.
Kayexalate enema: 15 to 60 g plus sorbitol given orally
or rectally as above.
Dialysis: If above therapy is unsuccessful, emergent dial-
ysis should be considered especially in patients with renal
failure even if not previously on dialysis.
C D
Prognosis
Severe hyperkalemia is the most fatal among all electrolyte
abnormalities and is a medical emergency. Overall prognosis
of hyperkalemia depends on the potassium level, efficacy of
therapy, and comorbidities associated with the hyper-
kalemia. The presence of diabetic ketoacidosis and renal fail-
ure as the cause of the hyperkalemia often confer a poor
prognosis.
Hypokalemia
Hypokalemia is defined as the presence of serum
potassium that is lower than normal. The normal value
for serum potassium is 3.3 to 5.3 mmol/L.
The most important ECG finding in hypokalemia is
the presence of prominent U waves. As the hy-
pokalemia becomes more profound, the amplitude of
the T wave becomes lower as the size of the U wave
becomes larger until both T and U waves bond to-
gether and become indistinguishable (Figs. 25.16 and
25.17).
Normal U wave: The U wave follows the T wave and is
the last component of ventricular repolarization. The
normal U wave is small measuring less than a quarter
of the size of the T wave. The exact origin of the normal
U wave is uncertain but is most probably from the re-
polarization of the Purkinje fibers.
Hypokalemic U wave: The U wave in hypokalemia is
large and pathologic. It is much larger than the T wave
and its origin is not the same as that of the normal U
wave. It has been shown that in hypokalemia, the nor-
mal T wave becomes interrupted, splitting into two
components. The T wave represents the first compo-
nent and the U wave the second component. Thus, the
Q-U interval truly represents the actual QT interval
and is prolonged. The QT interval represents only the
first component of the split T wave, and is equal to or
even shorter than the normal QT interval (Figs.
25.1825.21).
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Electrolyte Abnormalities 405

Figure 25.17: Prominent U Waves in Hypokalemia. Potassium level is 2.7 mm/L.The 12-lead electrocardio-
gram shows the classical finding of hypokalemia characterized by prominent U waves (arrows). Fusion of the T and
U waves is seen in V3; thus, the T and U waves become indistinguishable.

Figure 25.18: The QT and the Q-U Interval in

Q-U Interval Hypokalemia. Lead V3 and lead II were simulta-
neously recorded. In lead II, the U waves are
separately inscribed from the T waves and the two
Lead V3 humps resemble the back of a camel. If the QT inter-
val is measured in lead II, the QT interval is short
since it represents only the first component of a split
T wave. It does not represent the real QT interval. In
U Wave V3, the U waves are very prominent and can not be
separated from the T wave.This QU interval
QT Interval represents the actual QT interval and is prolonged.
The 12-lead electrocardiogram is shown in Figure
Lead II 25.17.

Figure 25.19: Prolonged QU Interval in Hypokalemia. Potassium level is 3.1 mmol/L.The U waves are
prominent in V26 with prolonged QU interval.
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406 Chapter 25

Figure 25.20: Prominent U Waves and Prolonged QU Interval in Hypokalemia. Potassium level is 2.8
mmol/L. The U waves are more prominent than the T waves and are most prominent in V3 to V5. The QU interval is
prolonged.

ECG Findings of Hypokalemia is decreased and the ratio between intracellular and extracel-
lular potassium becomes higher. Thus, the cells become more
1. Prominent U waves negative than 90 mV and the resting potential is hyperpo-
2. Nonspecific ST depression and T-wave flattening as the U larized. This will cause lengthening of the duration of the ac-
wave becomes more prominent tion potential resulting in a longer QT interval in the surface
3. Prolongation of the QU interval ECG. This will increase the frequency of ventricular arrhyth-
4. Fusion of the T and U waves mias especially torsade de pointes.
The ECG hallmark of hypokalemia is the presence of promi-
5. Ventricular arrhythmias, especially torsade de pointes
nent U waves and prolongation of the QU interval. As hy-
pokalemia worsens, the T wave flattens, a U wave emerges,
Mechanism and a seesaw effect between the amplitude of the T and U
wave occurs. As the U wave grows larger, the T wave be-
The ratio between intracellular and extracellular potassium comes smaller. Merging of the T and U waves eventually oc-
determines the resting potential of a cell, which is normally cur; thus, the T and U waves become indistinguishable from
90 mV. When there is hypokalemia, extracellular potassium one another.

Figure 25.21: Hypokalemia with "Roller Coaster" ST-T Configuration. Potassium level is 1.7 mmol/L.The T
waves have merged with the U waves in V46. The QU interval is prolonged with a roller coaster configuration in V26.
LWBK271-C25_396-413.qxd 29/1/09 7:20 pm Page 407 LWBK270-4119G-C02_073-110.qxd
In hypokalemia, phase 3 of the transmembrane action poten-
tial is less steep causing a small or attenuated intramyocardial
voltage gradient, resulting in low T waves. This is opposite to
that of hyperkalemia, where phase 3 has a steeper slope, which
translates into a higher intramyocardial voltage gradient, re-
sulting in T waves that are taller and more peaked.
According to Yan et al., the mechanism of a pathologic U
wave resulting from hypokalemia is different from the mech-
anism of a normal U wave. When hypokalemia is present, the
abnormal T-U complex has been shown to be due to splitting
of the ascending limb of the normal T wave into two compo-
nents. The first component of the split T wave is the original
T wave and the other component becomes a separate U wave,
which is actually the other half of the split T wave. If only the
QT interval is measured, which represents only the first com-
ponent of the bifid T wave, the QT interval is equal to or even
shorter than the normal QT interval. Thus, in hypokalemia,
measurement of the true QT interval should include the U
wave and is measured as the QU interval.
Clinical Implications
The normal level of potassium in the blood is 3.3 to 5.3
mmol/L. Hypokalemia refers to the presence of lower than
normal potassium in the blood, which is 3.3 mmol/L.
The normal daily intake of potassium varies from 80 to 120
mEq/day. Almost 90% of dietary potassium is excreted by the
kidneys and the rest by the gastrointestinal (GI) tract.
Hypokalemia usually occurs from potassium loss in the kid-
neys, frequently brought about by chronic diuretic therapy
or potassium loss in the GI tract as a result of frequent vom-
iting, continuous gastric suction, or diarrhea.
Hypokalemia also occurs when there is acute shift of extracel-
lular potassium intracellularly from metabolic alkalosis or
drugs such as insulin and beta agonists. Alkalosis causes extra-
cellular potassium to move into the cell in exchange for H, re-
sulting in a lower level of serum potassium. Metabolic alkalosis
decreases serum potassium by 0.8 mmol/L for every 0.1 unit in-
crease in pH above normal. Acidosis causes a reverse effect with
intracellular potassium moving out of the cell in exchange for
H. Thus, an acidotic patient with a normal potassium level is
expected to develop hypokalemia once the acidosis is corrected.
Symptoms of hypokalemia usually occur when significant elec-
trolyte depletion has occurred. This is usually manifested as
generalized weakness, fatigue, and paralysis. In patients who are
being weaned off a respirator, it is important that potassium
level should be checked because hypokalemia can cause muscle
weakness that can result in respiratory failure. If hypokalemia is
present, the electrolyte abnormality should be corrected. Hy-
pokalemia can affect the muscles of the GI tract, resulting in
ileus or constipation. It can also affect the muscles of the lower
extremities, resulting in leg cramps and paresthesias.
Arrhythmias including torsade de pointes and pulseless elec-
trical activity may occur when the QT (or QU) interval is
prolonged.
Electrolyte Abnormalities 407
Therapy
Because potassium is predominantly an intracellular ion, hy-
pokalemia may occur even when total body potassium is
normal or higher than normal. Generally however, when hy-
pokalemia is present and is from chronic loss of potassium, a
decrease in serum potassium of 1 mmol/L is equivalent to a
deficit of approximately 150 to 400 mmol of body potassium.
Therapy of hypokalemia includes identification and correc-
tion of the underlying abnormality.
Aggressive intravenous replacement of potassium may be as-
sociated with hyperkalemia and cardiac arrhythmias. Thus,
intravenous administration of potassium is preferred when
arrhythmias are present or when hypokalemia is severe
(2.5 mEq/L). Oral replacement is given if the patient is
clinically stable without arrhythmias and the potassium level
is 2.5 mmol/L because administration of potassium orally
is much safer and can be given in higher doses.
Replacement therapy of approximately 200 to 300 mmol
potassium is needed to increase the serum potassium level by
1 mmol/L. However, it may take several days to correct the
electrolyte abnormality because the administered potassium
is also excreted in the urine. Since intravenous replacement
of potassium can potentially cause cardiac arrhythmias, the
AHA guidelines recommend the following:
The maximum infusion of potassium should not exceed
10 to 20 mmol/hour and should be infused under contin-
uous cardiac monitoring.
Potassium when given 20 mmol/hour should be infused
with a central line. This concentration of potassium may
be painful when given IV because it may cause sclerosis of
the veins. The tip of the central catheter should not ex-
tend to the right atrium or ventricle because this may
cause local hyperkalemia.
If severe life-threatening arrhythmias are present and a more
rapid infusion is necessary, an initial infusion of 10 mmol
IV is given over 5 minutes and repeated once if necessary.
Potassium is preferably mixed with non-glucose solutions to
prevent insulin secretion, which can shift potassium intra-
cellularly.
Hypokalemia is usually associated with other electrolyte ab-
normalities, especially hypomagnesemia. When there is hy-
pomagnesemia, it might be difficult to correct the potassium
deficiency because magnesium is necessary for the move-
ment of electrolytes in and out of the cell including potas-
sium; therefore, correcting both electrolyte abnormality
should be done simultaneously.
The use of potassium sparing diuretics should be considered
in hypokalemic patients requiring long term diuretic therapy.
Prognosis
Hypokalemia can cause ventricular arrhythmias and may be
fatal if left uncorrected. It is usually from aggressive use of
diuretics or gastrointestinal losses. Unlike patients with
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408 Chapter 25

The ECG findings of hypercalcemia include (Figs.

A B
25.22 and 25.23):
Shortening of the QT interval. This is due to short-
ening of phase 2 of the action potential correspon-
ding to the ST segment in the ECG.
C
Elevation of the ST segment especially in the precordial

Figure 25.22: The Electrocardiogram of Hypercalcemia.
Diagrammatic representation of the electrocardiogram changes
associated with hypercalcemia. (A) Normal. (B) Hypercalcemia:
the ST segment is shortened because of shortening of phase
2 of the action potential. (C) Hypercalcemia with ST segment
elevation. Fusion of the QRS complex and T wave occur due to
further shortening of the ST segment.
hyperkalemia, the renal function in hypokalemic patients is
usually preserved. After the hypokalemia is corrected,
prognosis will depend on the underlying cause of the
hypokalemia.
leads. This may be mistaken for acute ischemic injury.
ECG Findings of Hypercalcemia
1. Short QT interval from shortening of the ST segment
2. Flattened and widened T wave with ST elevation
3. Prolonged P-R interval
4. Widened QRS complex
5. Increased QRS voltage
6. Notching of the terminal portion of the QRS complex from a
prominent J wave
7. AV block progressing to complete heart block and cardiac ar-
rest when serum calcium 15 to 20 mg/dL.

Mechanism
Hypercalcemia
Hypercalcemia refers to the presence of elevated cal-
cium level above normal. The normal level of total
serum calcium varies from 8.5 to 10.5 mg/dL or for
ionized calcium 4.2 to 4.8 mg/dL.
When extracellular calcium is increased, the duration
of the action potential is shortened. Shortening of the
action potential duration results in shortening of the
QT interval.
Increasing levels of serum calcium may cause changes in the
ECG. Unlike hyperkalemia, in which the ECG changes are
more dramatic, the ECG abnormalities associated with hy-
percalcemia are less specific and should not be used as the
basis for making the diagnosis of hypercalcemia.
Hypercalcemia shortens the duration of the action poten-
tial of the myocyte, resulting in a shortened QT interval.
This usually occurs when the serum calcium is 13 mg/dL.
Because the duration of ventricular systole is short-
ened, ventricular refractoriness is shortened, rendering the

Figure 25.23: The ST and T Wave Configuration in Hypercalcemia. Total calcium level is 16.0 mg/dL.
Note the short ST segment and ST elevation in V3 to V6. Prominent J wave or Osborn wave may also occur when
there is hypercalcemia.
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patient more prone to arrhythmias. It also renders patients
more susceptible to the toxic effects of digitalis.
Hypercalcemia initially increases inotropicity and chrono-
tropy by causing increased calcium influx and decreases
calcium egress in the myocyte. However, as serum calcium
further increases to levels 15 to 20 mg/dL, myocardial
contractility becomes depressed.
Very high levels of calcium, 15 to 20 mg/dL, may result
in arrhythmias most commonly bradycardia and com-
plete heart block.
Clinical Significance
Calcium is the most common mineral in the body; 99% of
the total amount of calcium is stored in bones. The remain-
ing 1% is distributed in the sera, 50% of which is bound to
albumin and the rest available as ionized calcium. Total
serum calcium is affected by the level of serum albumin.
When serum albumin is low, total calcium is low. Inversely,
when serum albumin is high, the total calcium level is high.
The level of ionized calcium, however, is not affected by the
level of serum albumin and is more important in causing
signs and symptoms of calcium excess or deficiency.
Pseudohypercalcemia can occur when there is profound de-
hydration, causing increased binding of calcium by albumin.
This will result in increased total serum calcium but the level
of ionized calcium remains normal. This can also occur in
some patients with multiple myeloma.
The normal level of total serum calcium is 8.5 to 10.5 mg/dL
and of ionized calcium 4.2 to 4.8 mg/dL. Hypercalcemia in-
dicates the presence of high levels of serum calcium above
the normal range. When real hypercalcemia is suspected, the
level of ionized calcium should be checked. Ionized calcium
is collected anaerobically, adjusted to a normal pH of 7.4, and
is often reported as normalized calcium.
The level of ionized calcium is actively regulated by the en-
docrine system. When there is hypocalcemia, enhanced se-
cretion of parathyroid hormone (PTH) increases osteoclastic
activity and bone resorption, thus increasing the level of cal-
cium in the blood. PTH also promotes absorption of calcium
in the GI tract by activating Vitamin D and decreases excre-
tion of calcium in the kidneys by promoting tubular reab-
sorption. Inversely, when there is increased level of calcium,
PTH secretion is inhibited and calcitonin is released, which
will lower serum calcium by reducing osteoclastic activity
and increasing the deposition of calcium in the bones and at
the same time increase excretion of calcium by the kidneys.
Ionized calcium is affected by pH, whereas total calcium is
not. When there is metabolic or respiratory alkalosis, H is
shifted from plasma proteins to serum to buffer the increased
bicarbonates. More ionized calcium will become protein-
bound to neutralize the more negatively charged plasma pro-
tein, thus decreasing the level of ionized calcium. The reverse
happens when there is acidosis: ionized calcium increases in
the serum.
Electrolyte Abnormalities 409
The two most common causes of hypercalcemia accounting
for more than 90% of cases are hyperparathyroidism and
malignancy.
Hyperparathyroidism may be primary from an au-
tonomously hyperfunctioning parathyroid gland (pri-
mary hyperparathyroidism) or secondary from chronic
renal disease (secondary hyperparathyroidism).
Hypercalcemia of malignancy is due to increased osteo-
clastic activity, resulting in increased bone resorption.
This may be due to increased hormonelike substances in
the blood or direct invasion of tumor cells into the bone.
n Humoral hypercalcemia: from increase in PTH-like
substances in the blood, resulting in increase osteoclas-
tic activity and bone resorption. This type of hypercal-
cemia is seen in squamous cell cancer of the lungs,
head and neck, and often renal and ovarian cancer.
n Bone metastasis: direct bone metastasis may also re-
sult in increased bone resorption most commonly the
result of breast cancer or multiple myeloma.
Other causes of hypercalcemia include use of drugs such
as thiazide diuretics, lithium, and vitamins A and D or
sarcoidosis and other granulomatous diseases.
There are usually no physical findings associated with the hy-
percalcemia itself. Symptoms of hypercalcemia usually do
not occur until the serum calcium reaches 12 mg/dL or
higher. Hypertension is common in patients with hypercal-
cemia and is a common manifestation in patients with pri-
mary hyperparathyroidism. At serum levels of 12 to 15 mg/dL,
weakness, apathy, fatigue, depression, and confusion may
occur. GI symptoms of constipation and dysphagia are
common. A higher incidence of dyspepsia and peptic ulcer
disease may occur because of a calcium-mediated increase in
gastrin secretion. As hypercalcemia becomes more severe,
dehydration may occur because hypercalcemia decreases
renal concentrating capacity, resulting in polyuria and poly-
dipsia. Finally, neurologic symptoms characterized by hallu-
cinations, disorientation, and coma may develop. Although
symptoms of hypercalcemia are usually neuromuscular,
cardiac manifestations may occur, including AV block and
cardiac arrest.
Therapy
Treatment is directed toward the underlying cause of the hy-
percalcemia. Therapy for hypercalcemia is essential when the
calcium level is 12 mg/dL, especially when the patient is
symptomatic. Therapy is mandatory at levels 15 mg/dL,
regardless of symptoms.
Excessive increase of calcium in the blood causes polyuria
and GI symptoms, especially in patients with malignancy,
resulting in dehydration. This enhances reabsorption of
calcium in the kidneys, thus further worsening hypercal-
cemia. Patients with hypercalcemia are therefore volume-
contracted; proper hydration with restoration of extracellular
volume promotes calcium excretion.
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410 Chapter 25

Saline diuresis: In symptomatic patients with severe hy- position that may not be ideally suited for rapid correction of
percalcemia 15 mg/dL who have reasonably preserved the electrolyte abnormality.
cardiovascular and renal function and are dehydrated, the
2005 AHA guidelines for cardiopulmonary resuscitation Prognosis
and emergency cardiovascular care recommends intra-
venous infusion of 300 to 500 mL/hour of 0.9% saline un- Prognosis depends on the underlying condition. Hypercal-
til any fluid deficit is corrected or until patient starts to cemia is commonly associated with malignancy; thus, the in-
diurese adequately. After the patient is properly hydrated, tensity of therapy should be individualized and should con-
IV hydration is continued at 100 to 200 mL/hour to main- sider the overall clinical picture.
tain adequate diuresis and promote calcium excretion. At
least 3 to 4 L is usually needed in the first 24 hours. Other
electrolytes, especially potassium and magnesium, should Hypocalcemia
be monitored carefully.
Loop diuretics: Loop diuretics (e.g., furosemide [2040
Hypocalcemia is defined as a calcium level below the
mg 2 to 4 times daily] or bumetanide [1 to 2 mg twice normal range. The normal serum calcium level varies
daily]), may be used in patients with heart failure, al- from 8.5 to 10.5 mg/dL and the normal level of ionized
though their use in the treatment of the hypercalcemia calcium is 4.2 to 4.8 mg/dL.
itself is controversial and should be used only after appro-
When the level of extracellular calcium is decreased,
priate volume repletion with normal saline. Thiazide
the following ECG changes occur:
diuretics should not be substituted for loop diuretics be-
The QT interval is prolonged. Prolongation of the QT
cause they prevent calcium excretion.

interval is due to prolongation of phase 2 of the ac-
Calcitonin: Calcitonin lowers serum calcium by inhibiting
tion potential, which corresponds to the ST segment
bone resorption and promoting urinary calcium excretion.
in the ECG. Thus, prolongation of the QT interval is
Bisphosphonates: Biphosphonic acid lowers serum cal- mainly due to prolongation of the ST segment. The T
cium by inhibiting osteoclastic bone resorption. The follow- wave is not significantly affected. Terminal inversion
ing bisphosphonates are commonly used in the treatment of of the T waves may occur (Figs. 25.2425.27).
hypercalcemia associated with malignancy.
Heart block may occur when the hypocalcemia is
Pamidronate: Pamidronate is given as an intravenous
more severe.
infusion. It can be combined with calcitonin to provide a
longer effect. There is risk of renal toxicity if given rapidly
or in high doses.
Zoledronic acid: Zoledronic acid is preferred as it is more
potent than pamidronate. It can be infused over a shorter A. Normal
period. The drug can also cause renal damage if the infu-
sion is given rapidly or in high doses. Renal function should
be reassessed if a second infusion is necessary. Patients re-
ceiving the infusion should be properly hydrated. Prolonged QU

Steroids: Glucocorticoids reduce calcium level by several

mechanisms. They inhibit intestinal absorption, increase uri-
nary excretion of calcium, and have cytolytic effect to some B. Hypokalemia The QT is prolonged
due to prominent U
tumor cells, especially multiple myeloma and other malig- wave
nancies. They also inhibit calcitriol production by mononu-
clear cells in lungs and lymph nodes; thus, they are effective
in hypercalcemia associated with granulomatous diseases
Prolonged ST
and occasionally with lymphoma. segment
Phosphates: Phosphates are given orally to prevent calcium C. Hypocalcemia QT is prolonged due
absorption. It combines with calcium to form complexes that to a wide ST segment

limits its absorption. It also increases calcium deposition in

bones.
Hemodialysis: Hemodialysis should be considered when
there is need to promptly decrease the level of serum calcium
in patients with heart failure or renal failure who cannot
tolerate saline infusion. The dialysis fluid should be altered
because the conventional dialysis solution may have a com-
Figure 25.24: The QT Interval of Hypocalcemia and
Hypokalemia. In hypokalemia, the prolongation of the QT or
QU interval is due to the presence of prominent U waves (B). In
hypocalcemia, prolongation of the QT interval is primarily due
to lengthening of the ST segment (C).
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Electrolyte Abnormalities 411

Figure 25.25: Prolonged ST Segment in Hypocalcemia. Total serum calcium is 7.6 mg/dL. The QT interval is
prolonged from lengthening of the ST segment. The T waves are narrow as shown in V4 to V6.

Figure 25.26: ST Segment and T Wave Changes Associated with Hypocalcemia. Serum calcium is 7.2
mg/dL.The QT interval is prolonged with ST depression and narrow T waves.

Figure 25.27: Hypocalcemia and Hyperkalemia. Potassium level is 5.6 mmol/L and total calcium is 6.8 mg/dL.
This electrolyte abnormality is commonly seen in renal failure.The T waves are peaked due to hyperkalemia and QTc
is prolonged measuring 491 milliseconds from hypocalcemia.
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412 Chapter 25
ECG Abnormalities of Hypocalcemia
1. Prolonged QT interval due to lengthening of the ST segment.
2. Flat ST segment and terminal T-wave inversion.
3. Heart block and ventricular fibrillation when hypocalcemia is
severe.
Mechanism
ECG findings include:
Prolongation of the QT interval. Prolongation of the QT
interval is due to lengthening of phase 2 of the action po-
tential. Because phase 2 of the action potential corre-
sponds to the ST segment, prolongation of the QT interval
is mainly from lengthening of the JT interval, which repre-
sents the interval between the end of the QRS complex and
the end of the T wave. Although the ST segment lengthens,
the size of the T wave is not altered. This is the most diag-
nostic ECG abnormality associated with hypocalcemia.
This is in contrast to hypokalemia where a prominent U
wave is present resulting in prolongation of the QT (QU)
interval. Other ECG findings include flat ST segment,
widening of the QRS complex, and AV block. Ventricular
fibrillation may occur when hypocalcemia is severe.
Therapy
Clinical Implications
Hypocalcemia refers to a low level of serum calcium below
the normal range of 8.5 to 10.5 mg/dL (or 2.1 to 2.6
mmol/L). It is also defined as below the normal level of ion-
ized calcium, which is 4.2 to 4.8 mg/dL (or 1.0 mmol/L).
The recommended daily calcium is 1,200 mg. Hypocalcemia
can occur when there is:
Decreased intake or diminished absorption of calcium: Vita-
min D is necessary for absorption of calcium in the GI tract.
Vitamin D deficiency can occur in patients who are not ex-
posed to sunlight or do not have adequate vitamin D in the
diet. In chronic renal failure, there is defective hydroxylation
of vitamin D to active vitamin D. Secondary increase in PTH
may occur in an effort to maintain serum calcium levels.
Parathyroid hormone deficiency: This is usually the result
of inadvertent removal of the parathyroid glands during
thyroid surgery. The parathyroid glands are also affected
by tumor or by infiltrative disorders, such as hemochro-
matosis or sarcoidosis.
Alkalosis: Metabolic or respiratory alkalosis decreases the
level of ionized calcium.
Chelation of calcium with citrate and other substances:
Hypocalcemia may occur following transfusion of 6 units
of citrated blood. Increased phosphates from acute renal
failure and exogenous bicarbonates and free fatty acids dur-
ing acute pancreatitis can also result in chelation of calcium.
Prognosis
Signs and symptoms of hypocalcemia are dependent not only
on the level of free or ionized calcium, but also on the rapid-
ity in which calcium declines. In renal patients, hypocalcemia
may not be clinically manifest because of coexistent acidosis,
which increases the level of ionized calcium and may abruptly
manifest only when the acidosis is corrected.
Symptoms of hypocalcemia usually do not occur until the
level of ionized calcium falls below 0.7 mmol/L. This includes
generalized irritability, hyperreflexia, muscle cramps, tetany,
carpopedal spasm, seizures, and neuromuscular excitability
characterized by a positive Chvostek and Trousseau signs.
Chvostek sign is elicited by tapping the facial nerve on the
face anterior to the ear resulting in twitching of the facial
muscles on the same side.
Trousseau sign involves inflating a blood pressure cuff above
the systolic pressure for 3 minutes, resulting in muscular
contraction with flexion of the wrist, thumbs, and metacar-
pophalangeal joints and hyperextension of the fingers.
Although symptoms of hypocalcemia are predominantly
neuromuscular and include weakness, tetany, confusion and
seizures, hypocalcemia can also cause arrhythmias, decrease
in myocardial contractility, heart failure, and hypotension.
Hypocalcemia usually develops in association with other
electrolyte abnormalities such as hyperkalemia and hypo-
magnesemia. The combination of hypocalcemia and hyper-
kalemia is commonly seen in patients with renal failure.
Treatment of hypocalcemia includes measurement of the
ionized level of serum. When symptoms are present, calcium
should be given intravenously even before the result of ion-
ized calcium is available. Between 100 and 300 mg of ele-
mental calcium is given intravenously, which will increase
serum calcium for 1 to 2 hours; thus, repeated doses may be
necessary. Calcium is given as calcium chloride or calcium
gluconate. Calcium chloride has a higher amount of elemen-
tal calcium compared to calcium gluconate:
Calcium chloride 10% 10 mL contains 360 mg of elemen-
tal calcium, whereas calcium gluconate 10% 10 mL con-
tains 93 mg of elemental calcium.
Calcium is given IV over 10 minutes (90 to 180 mg ele-
mental calcium) followed by an IV drip of 540 to 720 mg
in 500 to 1,000 mL D5W. The serum calcium level should
be monitored every 4 to 6 hours and maintained at the
low normal range of 7 to 9 mg/dL.
Calcium should be injected cautiously to patients receiv-
ing digitalis because it may cause digitalis toxicity.
If symptoms are not present, oral calcium supplements 1 to
4 g daily in divided doses may suffice.
Therapy includes correction of other electrolyte abnormali-
ties because calcium entry into the cells is dependent on the
presence of normal levels of magnesium and potassium.
Prognosis of patients with hypocalcemia will depend on the
underlying medical condition.
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Suggested Readings
2005 American Heart Association guidelines for cardiopul-
monary resuscitation and emergency cardiovascular care.
Part 10.1: life-threatening electrolyte abnormalities. Circula-
tion. 2005;112:IV-121I-125.
Agus ZS. Etiology of hypercalcemia. 2008 UpToDate. www.utdol.
com.
Agus ZS, Berenson JR. Treatment of hypercalcemia. 2008
UpToDate. www.utdol.com.
Dagogo-Jack S. Mineral and metabolic bone disease. In: Carey
CF, Lee HH, Woeltje KF, eds. The Washington Manual of
Medical Therapeutics. 29th ed. Philadelphia: Lippincott
Williams & Wilkins; 1998:441455.
Gibbs MA, Wolfson AB, Tayal WS. Electrolyte disturbances. In:
Marx JA, ed. Rosens Emergency Medicine, Concepts and Clinical
Practice. 5th ed. St. Louis: Mosby; 2002:17241744.
Inzucchi SE. Understanding hypercalcemia. Postgrad Med. 2004;
115:6976.
Palmer BF. Managing hyperkalemia caused by inhibitors or the
renin-angiotensin-aldosterone system. N Engl J Med. 2004;
351:585592.
Electrolyte Abnormalities 413
Rose BD. Clinical manifestations and treatment of hyper-
kalemia. 2008 UpToDate. www.utdol.com.
Rose BD. Clinical manifestations and treatment of hypokalemia.
2008 UpToDate. www.utdol.com.
Rutecki GW, Whittier FC. Recognizing hypercalcemia: the
3-hormone, 3-organ rule. J Crit Illness. 1998;13:5966.
Singer GG. Fluid and electrolyte management. In: Carey CF, Lee
HH, Woeltje KF, eds. The Washington Manual of Medical
Therapeutics. 29th ed. Philadelphia: Lippincott Williams &
Wilkins; 1998:3960.
Urbano FL. Signs of hypocalcemia: Chvosteks and Trousseaus
signs. Hosp Physician. 2000;36:4345.
Yan GX, Shimizu W, Antzelevitch C. Cellular basis for the nor-
mal T-wave and the electrocardiographic manifestations of
the long-QT syndrome. Circulation. 1998;98:19211927.
Yan GX, Lankipalli RS, Burke JF, et al. Ventricular repolariza-
tion components of the electrocardiogram, cellular basis
and clinical significance. J Am Coll Cardiol. 2003;42:
401409.
Zaloga GP, RR Kirby, WC Bernards, et al. Fluids and elec-
trolytes. In: Civetta JM, Taylor RW Kirby RR, eds. Critical
Care. 3rd ed. Philadelphia: Lippincott-Raven Publishers;
1997:413429.
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26
The ECG of Cardiac Pacemakers
Types of Pacemakers
Most physicians or paramedical personnel who are not fa-
miliar with artificial pacemakers will find any discussion
on cardiac pacemakers difficult and complicated. This
chapter will provide a simplified and basic discussion of
the electrocardiogram (ECG) of cardiac pacemakers.
Artificial cardiac pacemakers are electronic devices
that were clinically introduced for the treatment of
symptomatic bradyarrhythmias. The device consists
of a generator and one or more electrodes. The gener-
ator includes the circuitry and power supply, which
are encased in a sealed container made of stainless
steel or titanium. It is usually the size of a cigarette
lighter and is implanted subcutaneously in the pec-
toral or subclavicular region. The generator is con-
nected to the heart by electrodes, which are inserted
transvenously into the right atrium, right ventricle, or
to both chambers.
Initial classification: Permanent cardiac pacemakers
were initially classified as atrial, ventricular, or dual
chamber pacemakers (Fig. 26.1).
Atrial: An atrial pacemaker is a single chamber de-
vice consisting of a generator with an electrode in-
serted into the right atrium.
Ventricular: A ventricular pacemaker is a single
chamber device consisting of a generator with an
electrode inserted into the right ventricle.
Figure 26.1: Diagrammatic Representation A B
of the Different Types of Pacemakers.
(A) atrial pacemaker. (B) ventricular pacemaker.
(C) Dual chamber pacemaker.
Single Chamber
Atrial Pacemaker
414
Dual chamber: A dual chamber pacemaker is a de-
vice with two separate electrodes: one in the right
atrium and the other in the right ventricle.
Ventricular Pacemakers
Single chamber ventricular pacemaker: A basic
knowledge of the function of a single chamber pace-
maker is essential. This will serve as a foundation in un-
derstanding the ECG of the more complicated devices.
Single chamber ventricular pacemakers were the earliest
pacemakers that were put into clinical use for the treat-
ment of complete atrioventricular (AV) block. These
electronic devices can initiate a ventricular rhythm by
emitting an electrical impulse directly to the ventricles.
The electrical impulse is represented in the ECG as a
vertical artifact. The presence of a pacemaker artifact
is a signal that the pacemaker has discharged and the
wide QRS complex that immediately follows indi-
cates that it has captured the ventricles (Figs. 26.2
and 26.3).
Atrial Pacemaker
Single chamber atrial pacemaker: An atrial pace-
maker can be identified in the ECG by the presence of
C
Generator Electrode
Single Chamber Dual Chamber
Ventricular Pacemaker Pacemaker
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B Captured Ventricular
A
Complex
Single Chamber
Ventricular pacemaker Pacemaker Artifact
Figure 26.2: Single Chamber Ventricular Pacemaker.
(A) Diagrammatic representation of a single chamber ventricu-
lar pacemaker. The electrocardiogram generated by a ventricu-
lar pacemaker is shown in (B). Arrow points to the pacemaker
artifact, which generates a wide QRS complex representing a
captured ventricular impulse.
a pacemaker artifact similar to that of a ventricular
pacemaker. The pacemaker signal however is immedi-
ately followed by a P wave (instead of a QRS complex),
which indicates that the pacemaker has captured the
atrium (Figs. 26.4 and 26.5).
Single chamber atrial pacemakers were clinically intro-
duced for the treatment of symptomatic bradyarrhyth-
mias resulting from sick sinus syndrome. When the
atrium is stimulated, the impulse can propagate to the
ventricles and AV synchrony is preserved. Atrial pacing
is, therefore, more physiologic than ventricular pacing.
Single chamber atrial pacemakers are indicated only
when AV conduction is intact. They are not indicated
for the treatment of complete AV block.
Sensing and Pacing Functions
Fixed rate pacemakers: The earliest implantable
pacemakers were capable only of stimulating the heart
by delivering electrical impulses to the ventricle or
atrium. They were not capable of recognizing or sens-
ing the patients spontaneous rhythm. The device
therefore did not have any sensing capabilities and dis-
Figure 26.3: Ventricular Pacemaker. Rhythm strip showing a ventricular pacemaker. Each pacemaker stimu-
lus (arrow) is followed by a wide QRS complex representing a pacemaker captured ventricular complex.
The ECG of Cardiac Pacemakers 415
A
B
Captured
atrial impulse Conducted
ventricular
impulse
Single Chamber
Atrial Pacemaker
Pacemaker Artifact
Figure 26.4: Single Chamber Atrial Pacemaker. (A) A
diagrammatic representation of an atrial pacemaker. (B) The
electrocardiogram generated by an atrial pacemaker.The pace-
maker stimulus is followed by a P wave, which represents a
pacemaker captured atrial complex. If atrioventricular conduc-
tion is intact, the P wave is followed by a normally conducted
QRS complex.
charged constantly regardless of the patients rhythm.
These pacemakers were called fixed rate or asynchro-
nous pacemakers (Fig. 26.6).
Demand pacemakers: To avoid competition between
the pacemaker and the patients own rhythm, the
second-generation pacemakers were equipped with a
sensing circuit capable of detecting (or sensing) the pa-
tients intrinsic ventricular or atrial impulses. When a
spontaneous ventricular or atrial complex is detected,
the pacemaker was inhibited from delivering a stimu-
lus (Fig. 26.7). These devices were called demand or
synchronous pacemakers.
Pacemaker Identification System
As pacemaker function became increasingly more ad-
vanced, a coding system was developed to identify the
different modes or functions that a pacemaker is capa-
ble of. The first universally accepted pacemaker coding
system was developed by the Intersociety Commission
on Heart Disease Resources. The initial coding system
consisted only of three letters, which identified the type
and basic function of the pacemaker.
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416 Chapter 26

Figure 26.5: Atrial Pacemaker. Rhythm strip showing an atrial pacemaker. Each pacemaker stimulus
(arrows) is followed by a P wave representing a pacemaker-captured atrial complex.

The first letter identifies the chamber paced. This
could be the A, atrium; V, ventricle; or D, dual (both
atrium and ventricle).
The second letter indicates the chamber sensed. This
could be the A, atrium; V, ventricle; D, dual (both
chambers); or the number 0, none.
The third letter describes the pacemaker response to
a sensed event that could be I, inhibited; T, triggered;
D, dual (atrial inhibited followed by ventricular trig-
gered); or the number 0, none.
Thus, a fixed-rate, single-chamber ventricular pace-
maker, which is a pacemaker without sensing capa-
bilities, is designated as V00 and a demand ventricu-
lar pacemaker, which has sensing capabilities, is a
VVI or VVT. The same modes can be applied to atrial
pacemakers; thus, a fixed rate, single chamber atrial
pacemaker is designated as A00 and a demand atrial
pacemaker, which has sensing capabilities, is AAI or
AAT.
The various modes or different types of pacemakers are
coded below (Table 26.1):
As pacemaker technology became more complex, the
North American Society of Pacing and Electrophysiol-
ogy and the British Pacing and Electrophysiology
Group expanded the pacemaker code from three to five
letters (Table 26.2).
The fourth letter identifies programmable features
of the pacemaker (P, programmability is simple. M,
multiprogrammable when three or more program-
mable features are present. C, communicating: the
pacemaker communicates by transmitting stored
information to a programmer as opposed to a pro-
grammer sending commands to the pacemaker. R,
rate modulating, the pacemaker has features capable
of increasing its rate automatically during stress or
exercise. 0, none.
The fifth letter identifies whether the pacemaker is
capable of terminating tachyarrhythmias (P, pacing
is used to terminate tachyarrhythmias; S, shock is
used to terminate tachyarrhythmias; D or dual, both
pacing and shock can terminate an arrhythmia).
Thus, a VVI pacemaker that has the capacity to vary its
rate is a VVIR and the same pacemaker that uses burst
pacing to terminate a tachyarrhythmia is a VVIRP.
Ventricular Pacemakers
There are three possible single chamber ventricular
pacemaker modes: V00, VVI, and VVT.
V00 mode: This is the code for a fixed rate ventricular
pacemaker.
The first letter, V, stands for ventricle, which is the
chamber paced. The second letter, 0, indicates
that the device has no sensing capabilities. The

Figure 26.6: Fixed Rate Ventricular Pacemaker. Fixed rate ventricular pacemakers do not have sens-
ing capabilities and stimulate the ventricles constantly (arrows), regardless of the patients underlying rhythm.
Rhythm strip shows a fixed rate ventricular pacemaker. Note that the pacemaker is firing constantly causing a
pacemaker stimulus to be delivered after a spontaneous ventricular complex (first star).The pacemaker
impulse was not captured (block arrow) because the ventricles are still refractory from the ventricular impulse.
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The ECG of Cardiac Pacemakers 417

Figure 26.7: Demand Ventricular Pacemaker. Demand ventricular pacemakers are capable of recogniz-
ing the patients intrinsic rhythm. When a spontaneous ventricular complex is detected (stars), the pacemaker is
inhibited from delivering a stimulus to the ventricle; thus, competition between the pacemaker and the
patients own spontaneous rhythm is prevented.

third letter characterizes the mode of response to The first letter, V, indicates that the ventricle is the
a sensed event. Because the pacemaker has no chamber paced. The second letter, V, means that the
sensing capabilities, the third letter is automati- device is capable of sensing intrinsic impulses from
cally 0. the ventricles. The third letter, I, indicates that the
V00, or fixed rate ventricular pacemaker, is the first pacemaker is inhibited (meaning that it will not de-
permanent pacemaker introduced for the treat- liver a ventricular stimulus) when it senses a ventric-
ment of symptomatic AV block. It stimulates the ular event.
ventricles at a constant rate regardless of the under- VVI pacing is an upgraded version of a V00 pace-
lying rhythm (Fig. 26.8). Because the pacemaker maker. It is capable not only of stimulating the ven-
does not have any sensing capabilities, competition tricles, but is also able to sense impulses originating
always occurs between the patients own intrinsic from the ventricles. When the pacemaker senses a
rhythm and that of the constantly delivered pace- native QRS complex, the pacemaker is inhibited
maker stimuli. As a result, some pacemaker im- from delivering a pacemaker stimulus. Thus, com-
pulses are delivered to the ventricle even when the petition between the patients rhythm and that of
ventricles are completely refractory. Other impulses the pacemaker is prevented (Fig. 26.10).
may occur at the end of the T wave of a sponta- VVI pacing is the most commonly utilized among
neous ventricular complex, which corresponds to the three ventricular pacemaker modes. Even in the
the vulnerable period of the cardiac cycle (Fig. era of modern dual chamber pacing, VVI pacing is
26.9). This can potentially precipitate a cardiac ar- the pacemaker mode of choice when there is com-
rhythmia. plete AV block and permanent atrial fibrillation
VVI mode: This is the code for a demand ventricular (Fig. 26.11).
pacemaker. Hysteresis: In VVI pacing, the interval between two
consecutive pacemaker stimuli is constant and is the
same as the interval between a sensed ventricular
complex and the next pacemaker stimulus (Fig.
26.12). VVI pacemakers, however, can be pro-
TABLE 26.1 grammed to have a much longer escape interval. This
longer escape interval is called hysteresis and is
Pacemaker Coding System shown in Figure 26.13.
Atrial Ventricular Dual Chamber Hysteresis was intended to give the patient a chance
Pacemaker Pacemaker Pacemaker to manifest his own rhythm, which is often more ef-
fective than an artificially paced rhythm. A long hys-
A00 V00 DDD D00
teresis should not be mistaken for pacemaker mal-
AAI VVI DVI VDD
AAT VVT DVT VAT
function.
DAT VDT Oversensing: In VVI pacing, the pacemaker is inhib-
ited when it senses a native QRS complex. The pace-
The first letter represents the chamber paced, the second letter the
chamber sensed, and the third letter the pacemaker response to a maker may also be inhibited by extraneous artifacts
sensed event. such as muscle tremors (myopotentials) or electromag-
A, atrial; V, ventricle; D, dual; 0, none; I, inhibited; T, triggered. netic interference, especially those generated by large
motors. This type of pacemaker inhibition other than
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418 Chapter 26

TABLE 26.2

NASPE/BPEG Generic Pacemaker Code

Position I II III IV V
Chamber(s) Chamber(s) Response Programmability, Antitachyarrhythmia
Category Paced Sensed to Sensing Rate Modulation Function(s)
0 0 0 0 0
A A T P P*
V V I M S*
D D D# C D*
R
Manufacturers S, single S, single
designation only (A or V) (A or V)
NASPE, North American Society of Pacing and Electrophysiology; BPEG, British Pacing and Electrophysiology Group; 0, none; A, atrium; V, ventricle;
D, dual (atrium  ventricle); T, triggered; I, inhibited; D#, dual (triggered  inhibited); P, simple programmable; M, multiprogrammable; C, communi-
cating; R, rate modulation; P*, pacing (antitachyarrhythmia); S*, shock; D*, dual (pacing and shock).

Figure 26.8: V00 or Fixed Rate Single Chamber Ventricular Pacemaker. V00 pacemakers operate very
satisfactorily when there is no competing rhythm as shown. Note that all pacemaker artifacts (arrows) are
captured by the ventricles resulting in wide QRS complexes.

Figure 26.9: V00 or Fixed Rate Ventricular Pacemaker. When fixed rate pacing is used, pacemaker
artifacts are delivered constantly regardless of the patients rhythm (arrows). If the patient has an intrinsic rhythm
(stars), some pacemaker artifacts may be delivered at end of the T wave of the preceding intrinsic QRS complex
(block arrows) corresponding to the vulnerable period of the cardiac cycle.

Figure 26.10: VVI Pacing. In VVI pacing, the pacemaker is capable of stimulating the ventricles and sensing
spontaneous ventricular impulses. The fourth complex is a spontaneous QRS complex (star), which was sensed by
the pacemaker and was inhibited from delivering a ventricular impulse.
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The ECG of Cardiac Pacemakers 419

920 560 440 1000 720 680 610

Figure 26.11: VVI Pacing and Atrial Fibrillation. The rhythm is atrial fibrillation. The pace-
maker was programmed to discharge at a rate of 60 beats per minute and was appropriately inhib-
ited by the first five ventricular complexes. After the fifth complex, a long pause followed, which
was appropriately terminated by a pacemaker stimulus resulting in a captured ventricular complex
(arrow). The long pause measured 1,000 milliseconds, equivalent to a heart rate of 60 beats per
minute. The numbers indicate the intervals in milliseconds between the ventricular complexes.

those due to the patients intrinsic rhythm is called
oversensing. Extraneous artifacts, especially those re-
sulting from electromagnetic interference, may inhibit
the pacemaker output because the pacemaker erro-
neously senses these extraneous artifacts as the pa-
tients intrinsic rhythm. Because these electrical arti-
facts have a faster rate than the programmed rate of the
pacemaker, the pacemaker is inhibited and is prevented
from delivering a pacemaker output. If the patient is
pacemaker-dependent, prolonged inhibition of the
pacemaker may result in syncope.
Oversensing has been minimized and is no longer a
problem with modern-day pacemakers with the use of
bipolar instead of unipolar electrodes and insulating
the pacemaker generator with a metallic shield to pre-
vent oversensing of myopotentials. Use of electro-
cautery close to the generator during surgery, however,
still poses a potential problem, which can inhibit a
pacemaker in VVI mode. This can be prevented by pro-
gramming the pacemaker to fixed rate mode before the
surgery. Applying a magnet over the generator when-
ever electrocautery is activated can also temporarily
convert the pacemaker from VVI mode to a fixed rate
or V00 mode (Fig. 26.14).
VVT mode: This is the code for a ventricular triggered
pacemaker.
The first letter, V, indicates that the ventricle is the
chamber paced. The second letter,V, means that the de-
vice is capable of sensing intrinsic impulses from the
ventricles. The third letter, T, indicates that the pace-
maker is triggered when it senses a ventricular event
(meaning that when a ventricular impulse is sensed,
the pacemaker will respond by delivering a stimulus).
When the pacemaker senses a native ventricular
complex, a pacemaker artifact is emitted, which is
buried within the sensed QRS complex (Fig. 26.15).
A triggered response is the pacemakers way of
acknowledging that the ventricular impulse was
sensed. A triggered response within the QRS com-
plex is harmless; however, the frequency of pace-
maker output is increased and is not energy efficient.
Its main advantage is that when there is oversensing
of myopotentials or extraneous artifacts, VVT
pacing may prevent asystole in patients who are

Interval 1 is the same as Interval 2 No hysteresis

Interval 1 Interval 2
Escape
Interval

Figure 26.12: VVI or Ventricular Demand Pacemaker. VVI pacemakers are capable of sensing sponta-
neous ventricular impulses (stars). When a ventricular impulse is sensed, the escape interval between a sponta-
neous ventricular complex and the next pacemaker spike (interval 1) is the same as the interval between two
consecutive pacemaker spikes (interval 2).
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420 Chapter 26

Hysteresis = Interval 1 > Interval 2

Interval 1 Interval 2
Escape Interval

Figure 26.13: Hysteresis. Hysteresis is present when the escape interval after a sensed impulse (interval 1)
is longer than the interval between two consecutive pacemaker stimuli (interval 2). The presence of hysteresis
should not be mistaken for pacemaker malfunction.

pacemaker-dependent by delivering a ventricular when a spontaneous atrial impulse is sensed (Fig.

output as opposed to a pacemaker in VVI mode,
which is inhibited by these extraneous artifacts.
Triggered responses are no longer used in single
chamber pacemakers, but are commonly used in
dual chamber pacing. For example, when one cham-
ber such as the atria senses a native atrial complex,
the dual chamber pacemaker is triggered to deliver
an output to the ventricles after a programmed in-
terval to preserve AV synchrony (see Dual Chamber
Pacemakers).
Atrial Pacemakers
Atrial pacemakers are similar to ventricular pacemak-
ers except that the pacemaker generator is connected to
the atrium instead of the ventricle.
A00 mode: A00 or fixed rate atrial pacemaker con-
tinuously stimulates the atrium regardless of the
atrial rhythm (Fig. 26.16).
AAI mode: In atrial demand pacemaker, the
pacemaker is inhibited from delivering a stimulus
26.17).
AAT mode: When the pacemaker is atrial triggered,
the pacemaker is required to deliver a stimulus coin-
ciding with the sensed P wave when a spontaneous
atrial complex is sensed (Fig. 26.18).
Pacemaker Electrodes
Pacemaker electrodes: Most pacemaker electrodes
are endocardial electrodes and are inserted transve-
nously into the right atrium or right ventricle. The
right atrial electrode is usually anchored to the right
atrial appendage and the ventricular electrode at the
apex of the right ventricle. In rare cases in which trans-
venous insertion is not possible, a myocardial or epi-
cardial lead is sutured into the atrial or ventricular my-
ocardium using a transthoracic or subcostal approach.
There are two types of pacemaker electrodes: bipolar
and unipolar.
Bipolar: A bipolar electrode has the stimulating
electrode (or cathode) at the tip of the catheter and
the negative electrode (or anode) just below the

Magnet On Magnet Off

Figure 26.14: Application of a Magnet. Application of a magnet to the pacemaker generator will con-
vert the device to a fixed rate mode. Thus, a VVI pacemaker is converted to a V00 pacemaker with application of
a magnet as shown above. After the magnet is taken off the pacemaker, the pacemaker reverts to a VVI mode.
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The ECG of Cardiac Pacemakers 421

Figure 26.15: VVT or Ventricular Triggered Pacemaker. A pacemaker in VVT mode paces the
ventricles. It can also sense spontaneous impulses from the ventricles. When a ventricular impulse is sensed, the
pacemaker is immediately triggered to deliver a pacemaker stimulus as shown by the second and fifth
complexes (stars). The triggered output is seen as an artifact buried within the patients own QRS complex.

1 2 3 4 5

Figure 26.16: Atrial Pacemaker in A00 Mode. A pacemaker in A00 mode constantly delivers an atrial
output regardless of the atrial rhythm. It is not capable of sensing any atrial impulse. The third pacemaker arti-
fact occurred after an intrinsic P wave and was not captured. The fourth pacemaker artifact was able to cap-
ture the atrium and the pacemaker induced P wave (arrow) was conducted to the ventricles resulting in a nor-
mally conducted QRS complex.

Figure 26.17: AAI or Atrial Demand Pacemaker. In AAI mode, the atrium is paced. When an atrial P
wave is sensed (star), the pacemaker is inhibited from delivering an atrial stimulus.

Figure 26.18: AAT or Atrial Triggered Pacemaker. A pacemaker in AAT mode is similar to a
pacemaker in AAI mode except that the pacemaker is triggered to deliver a pacemaker stimulus (star) when
it senses an atrial event.
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422 Chapter 26
Figure 26.19: Bipolar and Unipolar Bipolar
Electrodes. (A) A bipolar electrode. Both positive Catheter
and negative electrodes are a short distance from
each other within the area of the right ventricle. (B) A
unipolar electrode.The stimulating electrode or cath-
ode is located at the tip of the catheter and the nega-
tive electrode is in the metal housing of the
pacemaker generator.
cathode at a distance of about 10 mm (Fig. 26.19A).
The short distance between the two terminals causes
a smaller pacemaker artifact in the ECG and a
smaller antenna effect; thus, the pacemaker is less af-
fected by electronic artifacts. Virtually all pacemak-
ers today have bipolar electrodes.
Unipolar: A unipolar electrode has the stimulating
electrode (or cathode) at the tip of the catheter and
Pacemaker Syndrome
the negative electrode (or anode) in the metal
housing of the pacemaker generator (Fig. 26.19B).
Because the flow of current extends from the apex
of the right ventricle (where the cathode is lo-
cated), to the pacemaker generator (where the an-
ode is located), the pacemaker artifact is unusually
large. The wide distance between the two elec-
trodes also causes a large antenna effect, rendering
the pacemaker vulnerable to interference by elec-
tromagnetic forces.
The location of the pacemaker electrode determines
the morphology of the QRS complex. Stimulation of
the right ventricle will result in a left bundle branch
block configuration of the QRS complexes (Fig. 26.20).
Stimulation of the left ventricle will generate a QRS
Figure 26.20: Right Ven-
tricular Pacing. When the
stimulating electrode is in the
right ventricle, the QRS com-
plexes have a left bundle
branch block configuration
with deep S waves in V1V2.
A B Unipolar
Catheter
Anode or
negative
electrode -
Cathode or
stimulating +
+ electrode
complex with a right bundle branch block configura-
tion (Fig. 26.21). Not all pacemaker-induced right
bundle branch block patterns are due to left ventricular
pacing, however.
Pacemaker syndrome: Symptoms of low output,
hypotension, and even syncope or near syncope can
occur in patients with cardiac pacemakers, especially
in VVI mode. This constellation of symptoms during
ventricular pacing is called the pacemaker syndrome.
Pacemaker syndrome can occur if there is retrograde
conduction of the ventricular impulse to the atria
(Fig. 26.22), causing both atria and ventricles to con-
tract simultaneously. When the atria contracts
against a closed mitral and tricuspid valves, pul-
monary venous hypertension, low cardiac output,
and reflex hypotension can occur. This can be mini-
mized with insertion of a dual chamber cardiac pace-
maker.
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The ECG of Cardiac Pacemakers 423

Figure 26.21: Left Ventric-

ular Pacing. A transvenous
catheter was inserted into the
left ventricle after inadvertently
crossing a patent foramen
ovale. Note that the QRS com-
plexes in V1 have right bundle
branch block configuration
indicative of left ventricular
pacing.

device because it combines atrial and ventricular sens-

Dual Chamber Pacemakers
Dual chamber pacemakers: Dual chamber pacing
was introduced to preserve AV synchrony. It has sepa-
rate electrodes, one in the ventricle and the other in the
atrium. Dual chamber pacing is easy to recognize in the
ECG when there are two separate pacemaker stimuli,
one capturing the atria and the other the ventricles. Its
function is more complicated than a single chamber
ing with atrial and ventricular pacing.
The different ECG patterns associated with a dual
chamber pacemaker are shown in Figure 26.23.
Atrial pacing in combination with ventricular pacing
Atrial pacing in combination with ventricular sensing
Atrial sensing in combination with ventricular
pacing
Atrial sensing in combination with ventricular sensing

Figure 26.22: Ventriculoatrial Conduction during VVI Pacing. Ventriculoatrial (V-A) conduction or conduc-
tion of the ventricular impulse to the atria can occur during ventricular pacing resulting in retrograde P waves. The
P waves are seen after the QRS complexes (arrows) and are due to retrograde conduction of the ventricular impulse
to the atria across the AV conduction system. Pacemaker syndrome is due to simultaneous contraction of both atria
and ventricles when there is V-A conduction. V-A conduction is possible even in patients with complete AV block.
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424 Chapter 26

B will be inhibited from discharging a pacemaker

Atrial Pacing and
Ventricular Pacing
A available pacemakers and was introduced to pre-
Atrial Pacing and
Ventricular Sensing
Atrial Sensing and
Ventricular Pacing
Dual Chamber
Pacemaker
Atrial Sensing and
Ventricular Sensing
Possible ECG of Dual Chamber Pacemaker
Figure 26.23: Dual Chamber Pacemaker. (A) A diagram-
matic representation of a dual chamber pacemaker. (B) The dif-
ferent electrocardiogram patterns associated with a dual cham-
ber pacemaker.
DDD Pacing
DDD Pacing: Among several dual chamber pacemaker
modes, DDD pacing is the most commonly used. It is
called universal pacemaker because it is the only pace-
maker that can pace and sense both chambers sepa-
rately. Figures 26.24 through 26.28 show the possible
ECG findings associated with DDD pacing.
In DDD pacing, the pacemaker is capable of sensing
impulses from both atrium and ventricle. When the
pacemaker senses an atrial impulse, the atrial chan-
nel is inhibited from delivering an atrial stimulus.
Inhibition of the atrial channel triggers the ventric-
ular channel to deliver a stimulus to the ventricle af-
ter a programmed interval. However, if a sponta-
neous ventricular impulse is sensed, the pacemaker
stimulus.
DDD pacing is the most physiologic among all
served AV synchrony.
Other ECG presentations of DDD pacing are shown in
Figs. 26.2626.28.
Indication: DDD pacing is the pacemaker mode of
choice when there is complete AV block with intact
sinus function. The pacemaker can track the atrial rate
and triggers a ventricular output for every atrial im-
pulse that is sensed. The pacemaker therefore is rate-
responsive because spontaneous increase in atrial rate
is always followed by a pacemaker-induced ventricular
response. Thus, when the patient develops sinus tachy-
cardia during stress or exercise, the ventricular rate in-
creases commensurately, because the pacemaker is
committed to deliver a ventricular output after every
sensed atrial event (Fig. 26.29).
Contraindication: DDD pacing, however, is not ap-
propriate for all clinical situations. Although DDD pac-
ing is the pacemaker mode of choice among patients
with complete AV block with intact sinus function, it is
contraindicated when there is permanent atrial fibrilla-
tion. DDD pacing is not appropriate when there is atrial
flutter or fibrillation because every sensed atrial event
will trigger a ventricular output (Figs. 26.30 and 26.31).
Furthermore, it is not possible to pace the atrium when
there is atrial flutter or atrial fibrillation. In this setting,
a VVI pacemaker is the pacemaker mode of choice.
Mode switching: When atrial flutter or fibrillation is
paroxysmal or recurrent, some DDD pacemakers are
capable of mode switching when the supraventricular
arrhythmia is detected. For example, in patients with
DDD pacemakers, the pacemaker mode switches auto-
matically from DDD to VVI mode when atrial fibrilla-
tion is detected and back to DDD when the arrhythmia
spontaneously converts to normal sinus rhythm. If a
DDD pacemaker is not capable of automatic mode
switching, it should be programmed to a VVI mode.

A A A
A A

V V V V
V

Figure 26.24: Dual Chamber Pacemaker without any Competing Rhythm. The presence of sepa-
rate atrial (A) and ventricular (V) stimuli suggest that the pacemaker is dual chamber. Atrial pacing followed by
ventricular pacing is one of the possible electrocardiogram patterns of a DDD pacemaker.
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The ECG of Cardiac Pacemakers 425

AP AP AP AP AP

VS VS VS VS VS

Figure 26.25: DDD Pacing: Atrial Pacing Followed by a Spontaneous Ventricular Rhythm. An-
other electrocardiogram pattern of DDD pacing is the presence of pacemaker induced atrial complexes, which
may conduct normally to the ventricles. The pacemaker senses the normally conducted ventricular complexes
(VS) resulting in inhibition of the ventricular output hence no ventricular pacemaker artifact is present. AP,
atrial pacing; VS, ventricular sensing.

Figure 26.26: DDD Pacing: Normal Sinus Rhythm followed by Paced Ventricular Rhythm.
DDD pacing can also present with sinus P waves followed by pacemaker-induced QRS complexes. When
sinus rhythm is present, the sensed P waves inhibit the atrial output and at the same time triggers the
pacemaker to deliver a ventricular output after a programmed atrioventricular interval. Thus, when sinus
tachycardia occurs, every P wave will be followed by a QRS complex.

Figure 26.27: DDD Pacing: Normal Sinus Rhythm with Normal Atrioventricular Conduction.
In DDD pacing, the presence of spontaneous atrial and ventricular complexes may inhibit the pacemaker
output completely. This will allow the patient to manifest his or her own rhythm without evidence of pace-
maker activity.

VP VP
AP AP VP AP AS AS

VS VS

Figure 26.28: DDD Pacing. This rhythm strip summarizes all the possible combinations for DDD pacing.
AP, atrial pacing; AS, atrial sensing; VP, ventricular pacing; VS, ventricular sensing.
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426 Chapter 26

Figure 26.29: Pacemaker in DDD Mode Tracking Sinus Tachycardia. Sinus tachycardia is present with
upright P waves in leads I, II, and aVF. DDD pacing can track the atrial rate committing the pacemaker to deliver a
ventricular output for every sensed atrial event. DDD pacing is the pacemaker of choice when complete
atrioventricular block is present with intact sinus node function.

Figure 26.30: DDD Pacing During Atrial Fibrillation. During atrial fibrillation, a pacemaker in DDD mode
can track the atrial rate and delivers a ventricular output after every sensed atrial event resulting in a fast ventricular
rate as shown above. DDD pacing therefore is not appropriate during atrial fibrillation. The pacemaker should be
programmed to a VVI mode. See also Figure 26.11.

Figure 26.31: DDD Pacing and Atrial Flutter. Rhythm strip A shows a dual chamber pacemaker in DDD
mode in a patient with atrial flutter. Note that the pacemaker rate is relatively fast at approximately 115 per minute.
Rhythm strip B was taken after the pacemaker was programmed to VVI mode.The rhythm is atrial flutter and the
ventricular rate is slower at 60 per minute.
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The ECG of Cardiac Pacemakers 427

Figure 26.32: Pacemaker-Mediated Tachycardia. Twelve-lead electrocardiogram of a patient with

pacemaker mediated tachycardia (PMT). PMT is possible only when there is ventriculoatrial (V-A) conduction
(arrows), which are seen as retrograde P waves in II, III, and aVF. The P waves are sensed by the atrial channel trigger-
ing the pacemaker to deliver a ventricular output. Once the ventricles are stimulated, V-A conduction again occurs
resulting in PMT.

If the pacemaker has to remain in DDD mode, the

Pacemaker-Mediated Tachycardia
Pacemaker-mediated tachycardia: One of the com-
plications of DDD pacing is pacemaker-mediated tachy-
cardia (PMT) (Fig. 20.32). This tachycardia is possible
only when there is ventriculoatrial (V-A) conduction.
V-A conduction refers to the conduction of an impulse
retrogradely from ventricles to atria through the AV con-
duction system. V-A conduction has been shown to oc-
cur even in the presence of complete AV block.
When the ventricle is paced, the ventricular impulse
can conduct retrogradely to the atria. The retrograde
P wave is sensed by the atrial channel of the pacemaker
and commits the pacemaker to deliver a ventricular
output, which will again result in retrograde conduc-
tion. PMT can also occur in any dual chamber pace-
maker in which a sensed atrial event can trigger a ven-
tricular output such as VDD, VAT, and DDT modes.
PMT can be terminated by placing a magnet over
the pacemaker generator, temporarily converting
the pacemaker to a fixed rate or D00 mode or by re-
programming the pacemaker.
PMT can also be terminated by programming the
pacemaker to DVI or VVI mode. Any programming
that renders the atrial channel incapable of sensing ret-
rograde P waves will terminate the tachycardia.
pacemaker can be reprogrammed not to recognize the
retrograde P wave. This is done by lengthening
the atrial refractory period (ARP). During the ARP,
the atrial channel is not able to sense any impulse
(Fig. 26.33). The atrial refractory period starts with a
paced or sensed atrial activity and continues until
ventricular pacing or sensing. The ARP also extends
beyond the QRS complex and is called postventricu-
lar atrial refractory period (PVARP). The duration of
the PVARP is programmable. The PVARP is built into
the pacemaker to prevent the atrium from sensing the
ventricular output and QRS complex as an atrial
event. Lengthening the PVARP will prevent the pace-
maker from sensing retrograde P waves because the
retrograde P wave will now fall within the atrial re-
fractory period.
An endless loop PMT should not be confused with si-
nus tachycardia during DDD pacing. When sinus
tachycardia is present, the P waves are upright in II, III,
and aVF (Fig. 26.34A). On the other hand, when PMT
is present, the P waves are retrogradely conducted
(ventriculoatrial conduction) and will be inverted in
leads II, III, and aVF (Fig. 26.34B).
Very often, a pacemaker tachycardia can also occur
when there is atrial flutter or atrial fibrillation (Figs.
26.30, 26.31, and 26.35).
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428 Chapter 26

TARP
Lengthening the PVARP
will prevent sensing of the
retrograde P wave
PVARP
ARP
Retrograde P Wave
Figure 26.33: Atrial Refractory Period in DDD Pacing.
The atrial refractory period (ARP) starts with atrial pacing and
continues until ventricular pacing or ventricular sensing. This
corresponds to the whole atrioventricular or PR interval and in-
dicates the time that the atrial channel is unable to sense any
impulse. The ARP also continues beyond ventricular pacing (or
sensing). This portion of the atrial refractory period is called the
postventricular atrial refractory period (PVARP).The length of
the PVARP is programmable. The total atrial refractory period
(TARP) includes the ARP and the PVARP. During the TARP, the
atrial channel is deft to any impulse. If there is PMT, the PVARP
can be programmed to a longer interval (dotted line) so that it
will not sense the retrograde P wave.
ECG Pattern of Other Dual
Chamber Pacemakers
The ECG of other, less commonly encountered dual
chamber pacemakers are shown.
VAT mode: The pacemaker is an atrial synchronous
pacemaker and was one of the earliest dual chamber
pacemakers introduced clinically that can preserve AV
synchrony (Fig. 26.36).
When an atrial impulse is sensed, the pacemaker is
triggered to deliver a pacemaker stimulus to the ven-
tricles. Thus, the ventricles are stimulated only when
a spontaneous atrial impulse is sensed. When there
is no spontaneous atrial rhythm, the pacemaker acts
like a V00 pacemaker because the pacemaker does
not sense ventricular impulses.
The main drawback of VAT pacing is that sensing
occurs only in the atrium. Thus, spontaneous
ventricular complexes are not sensed and the
pacemaker can deliver electrical stimuli to the
ventricles even when there are spontaneous QRS
complexes.
DVI Pacing: Also called A-V sequential pacing. It was
intended for patients with complete AV block (Fig.
26.37).
When the pacemaker senses a spontaneous ventric-
ular complex, the pacemaker is inhibited from deliv-
ering a stimulus to the ventricles. Thus, the initial
pacemaker stimulus is delivered to the atrium after a
programmed escape interval. This interval is meas-
ured from the last spontaneous or pacemaker in-
duced ventricular complex. After the atrium is
paced, the ventricle is sequentially paced; however, if
a spontaneous ventricular impulse is sensed, the
pacemaker stimulus will be inhibited.
Unlike VAT pacing in which the ventricles are stimu-
lated even when a spontaneous ventricular complex
is present, pacing in DVI mode prevents the pace-
maker from delivering a stimulus to the ventricle if
the pacemaker senses a spontaneous ventricular im-
pulse. Because DVI pacing is not capable of sensing
atrial impulses, AV synchrony is not preserved.
VDD mode. In VDD mode, only the ventricle is
paced. Sensing occurs in both chambers. The pace-
maker is not capable of pacing the atrium; however,
when an atrial impulse is sensed, the pacemaker
is triggered to deliver a ventricular output. If the

Sinus P waves are upright in II

Retrograde P waves are inverted in II

A B

Figure 26.34: DDD Pacing During Sinus Tachycardia (A) and Endless Loop
Tachycardia (B). (A) Sinus tachycardia with P waves upright in lead II (arrows). The full
12-lead electrocardiogram (ECG) of sinus tachycardia followed by pacemaker induced ventric-
ular response is shown in Figure 26.29. (B) Endless loop pacemaker mediated tachycardia.The P
waves are inverted in lead II (arrows). The full 12-lead ECG of a pacemaker mediated tachycardia
is shown in Figure 26.32.
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Lead II A Lead II B

Figure 26.35: DDD Pacing with Mode Switching. (A) A dual chamber pacemaker
in DDD mode. Ventricular pacing is seen with a rate of approximately 110 beats per minute,
which is the maximum rate that is programmed for the pacemaker. The underlying rhythm
is not obvious in the rhythm strip. Because the pacemaker is capable of mode switching, it
automatically programs itself into a VVI mode (B) with a rate of approximately 70 beats per
minute.The underlying rhythm is atrial flutter with atrioventricular block.The flutter waves
are marked by the arrows.

1 2 3 4 5 6 7 8

Figure 26.36: VAT mode. VAT pacing is the first atrial sensing dual chamber
pacemaker put into clinical use that is capable of preserving atrioventricular (AV)
synchrony. In VAT pacing, the ventricle is the only chamber paced and the atrium is the
only chamber sensed. When a spontaneous atrial impulse is sensed, the ventricle is trig-
gered after a programmed AV interval (first, second, fourth, and seventh complexes),
thus the pacemaker can track the atrial rate and is rate responsive. Because a sensed P
wave always triggers a ventricular output, AV synchrony is preserved. The drawback is
that competition can occur when spontaneous ventricular rhythm is present because
the pacemaker is not capable of sensing ventricular impulses (fifth and eighth
complexes). When there is no atrial activity (third complex), the pacemaker will function
in V00 mode. Arrows point to the pacemaker artifacts.

1 2 3 4 5 6
A V A V A A V
A

Figure 26.37: DVI Mode. In DVI pacing, both atria and ventricles are paced. The ventri-
cle is the only chamber sensed. In the absence of a competing rhythm, the atrium and ven-
tricle are sequentially paced and the resulting electrocardiogram is shown in complexes
1 and 2.When a native ventricular impulse is sensed, the ventricular output is inhibited
(third, fourth, and fifth complexes).When the ventricular rate drops below a preset rate
(distance between third and fourth complexes), the pacemaker is committed to deliver an
atrial output regardless of the atrial rhythm. Note that the atrial artifact in four was not fol-
lowed by a ventricular output because the pacemaker was able to sense the native ventric-
ular complex. It was not able to recognize the P wave in front of the QRS complex because
DVI pacing is not capable of sensing atrial impulses (fourth complex). The pacemaker is
not rate responsive since the pacemaker is not capable of sensing atrial impulses; thus,
atrioventricular synchrony is not preserved. The arrows identify the pacemaker artifacts.
(A represents atrial pacemaker artifacts and V represent ventricular pacemaker artifacts).

429
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430 Chapter 26

1 2 3 4 5 6

Figure 26.38: VDD Mode. In VDD mode only the ventricle is paced. The pacemaker is
capable of sensing impulses from both atrium and ventricle (first two complexes). When
an atrial impulse is sensed, the pacemaker is triggered to deliver a ventricular output after
a programmed atrioventricular (AV) interval (third and fourth complexes). When a ventricu-
lar complex is sensed, the pacemaker is inhibited from delivering a ventricular output (fifth
complex). When the atrial rate is fast, the pacemaker can track the atrial rate and is therefore
rate responsive similar to a DDD pacemaker. However, when the atrial rate is unusually slow
or when there is no atrial activity (pause after the fifth complex), the pacemaker functions
in the VVI mode (sixth complex) because the pacemaker is not capable of pacing the
atrium and loses its advantage as a dual chamber pacemaker in preserving AV synchrony.

pacemaker senses a spontaneous ventricular complex, it
is inhibited from delivering a pacemaker stimulus to the
ventricles. The pacemaker will function as a VVI pacer if
it does not sense any spontaneous atrial complex (Fig.
26.38).
DDI pacing: In DDI pacing, the atrial or ventricular out-
puts are inhibited when atrial or ventricular impulses are
sensed. Although atrial sensing occurs, the pacemaker is
not triggered to deliver a ventricular stimulus, thus the
pacemaker is not rate responsive (Fig. 26.39).
terminating ventricular tachycardia with burst pacing.
This is usually accomplished by delivering a series of
ventricular pacemaker stimuli in an attempt to capture
the ventricles during the tachycardia. Figure 26.40
shows ventricular tachycardia terminated successfully
by burst pacing.
In Figure 26.41, burst pacing was delivered inappropri-
ately during a sinus tachycardia, which was mistaken
for ventricular tachycardia. After burst pacing was
completed, the rhythm had deteriorated from sinus
tachycardia to ventricular tachycardia.

Pacemaker with Antitachycardia

Properties
Pacemakers are also capable of terminating ventricular
tachycardia. The rhythm strips in Figures 26.40 and
26.41 show a VVIRP pacemaker, which is capable of
Biventricular Pacemakers and
Cardioverter Defibrillators
Biventricular pacemakers: Patients with wide QRS
complexes resulting from left or right bundle branch

3 5
1 2 4 6

Figure 26.39: DDI mode. Both atrium and ventricle are paced (first two complexes).
The pacemaker is capable of sensing impulses from both atrium and ventricle. When an
atrial impulse is sensed (star), the pacemaker is inhibited from delivering an atrial output.
When a ventricular impulse is sensed (third and fifth complexes), the pacemaker is
inhibited from delivering a ventricular output. When the atrial rhythm is unusually slow or
when there is no atrial activity (pause after the fifth complex), atrial pacing is initiated when
the lower rate limit of the pacemaker is reached (sixth complex). This is followed by a ven-
tricular output unless a spontaneous ventricular complex occurs. Although the pacemaker
is capable of sensing atrial impulses, the ventricular output is not triggered when an atrial
impulse is sensed (star). The pacemaker therefore is not rate responsive since it is not capa-
ble of increasing the ventricular rate when the atrial rate increases during stress or exercise.
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The ECG of Cardiac Pacemakers 431

Ventricular Tachycardia Overdrive Pacing

Normal Sinus Rhythm

Figure 26.40: Overdrive Pacing Terminating Ventricular Tachycardia. The left side of the tracing
shows ventricular tachycardia with a rate of 180 beats per minute. The pacemaker recognizes the ventricular
tachycardia and delivers a burst of ventricular pacemaker stimuli, which is faster than the rate of the ventricu-
lar tachycardia. The pacemaker successfully captures the ventricles during pacing. When pacing is terminated,
the rhythm is successfully converted to a slower ventricular rhythm followed by normal sinus rhythm.

block, severe left ventricular systolic dysfunction (ejec-
tion fraction 35%), and symptoms of heart failure in
spite of optimal medical therapy are candidates for im-
plantation of biventricular pacemakers. Biventricular
pacing is performed by pacing both ventricles simultane-
ously, even in the absence of bradyarrhythmias from AV
block or sinus node dysfunction. Biventricular pacing
synchronizes ventricular contraction in patients with
bundle branch block and has been shown to improve
cardiac output in patients with wide QRS complexes who
also have severe left ventricular dysfunction. The left ven-
tricle is paced with an electrode inserted through the
coronary sinus. The right atrium and right ventricle are
paced conventionally. Patients with severe left ventricular
dysfunction are also at risk for malignant ventricular ar-
rhythmias. Thus, patients with heart failure requiring
biventricular pacemakers are also candidates for implan-
tation of devices with defibrillating properties.
Automatic implantable devices: Patients who are
survivors of cardiac arrest or patients who are high risk
for ventricular tachycardia or fibrillation are candi-
dates for implantation of automatic cardioverter defib-
rillators. These devices are commonly integrated with
biventricular pacemakers in patients undergoing car-
diac resynchronization therapy. Thus, automatic im-
plantable defibrillators are commonly integrated with
pacemakers and permanent pacemakers are integrated
with defibrillating properties, making them capable of
treating both bradycardia and tachycardia. An example
of a patient with an implantable cardioverter/defibrilla-
tor (ICD) whose ventricular tachycardia is terminated
by delivery of an electrical shock is shown in Figure
26.42. Although the defibrillator also has pacemaking
properties, pacemaker activity was not necessary after
successful cardioversion.
Artificial Cardiac Pacemakers:
Clinical Implications
Permanent pacemakers were clinically introduced for the
treatment of symptomatic bradyarrhythmias from complete
AV block and sinus node dysfunction. Single chamber ven-
tricular pacemakers were the first generation of implantable
devices used for this purpose. Single chamber ventricular
pacemakers, however, do not preserve AV synchrony. Further-
more, ventricular pacing can result in pacemaker syndrome.

Sinus Tachycardia Mistaken for

Ventricular Tachycardia Overdrive Pacing Ventricular Tachycardia

Figure 26.41: VVIRP. Rhythm strip shows a rate responsive VVI pacemaker with features capable of
terminating a tachyarrhythmia using burst pacing (VVIRP). In the rhythm strip, the pacemaker mistook
the sinus tachycardia for ventricular tachycardia and inappropriately delivered a burst of 10 ventricular
pacemaker stimuli, which is successful in capturing the ventricles. When pacing was terminated, the
rhythm had changed to ventricular tachycardia as noted at the end of the rhythm strip.
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432 Chapter 26
Figure 26.42: Automatic Implantable Cardioverter Defibrillator (AICD). Rhythm strip showing a wide
complex tachycardia on the left half of the rhythm strip.The AICD was able to recognize the ventricular tachycardia
and automatically delivered an electrical shock (arrow) that successfully converted the rhythm to normal sinus (right
side of the tracing).
Pacemaker syndrome is a hemodynamic consequence of
ventricular pacing. This is mainly from retrograde or ven-
triculoatrial conduction of the paced ventricular impulse to
the atria. This is characterized by cannon A waves in the neck
from contraction of the atria when the mitral and tricuspid
valves are closed. Increase in atrial and pulmonary venous
pressures can occur when the atria are contracting against a
closed AV valve, resulting in shortness of breath as well as re-
flex drop in blood pressure. This overall symptom complex
of hypotension, shortness of breath, and low cardiac output
is called the pacemaker syndrome.
Single chamber ventricular pacemakers have been replaced
by dual chamber pacemakers, which are more physiologic,
because AV synchrony is preserved. Although single channel
AAI pacemakers can also preserve AV synchrony, they are
limited to patients with intact AV conduction and are not in-
dicated in the presence of complete AV block. VVI pacemak-
ers remain the most commonly implanted pacemaker world-
wide. In the United States, most pacemakers that are
implanted are dual chamber devices in DDD mode.
VVI pacing continues to be the pacemaker mode of choice
when complete AV block occurs in the setting of permanent
atrial fibrillation. DDD pacing is contraindicated because it
is not possible to pace the atrium when there is atrial flutter
or fibrillation. Furthermore, the presence of atrial flutter or
fibrillation will commit the pacemaker to deliver a ventricu-
lar output for every sensed atrial event resulting in unneces-
sary tachycardia.
Although single chamber atrial pacemaker is the most ap-
propriate device for patients with sick sinus syndrome, dual
chamber pacing in DDD mode is more often used. Sick sinus
syndrome is most commonly the result of degenerative dis-
ease that affects not only the sinus node but may eventually
involve the AV node and distal conduction system.
Pacemakers are sometimes inappropriately inhibited by extra-
neous impulses such as muscle tremors, electrocautery, mi-
crowaves, magnetic fields, and other artifacts. Oversensing of
these artifacts has been minimized with the use of bipolar elec-
trodes where the anode or negative electrode is mounted just a
short distance from the tip of the catheter thus shortening the
distance between the two electrodes and the size of the antenna.
If electrocautery is performed during a surgical procedure, it
should not involve the area of the pacemaker generator. If this
cannot be avoided, the pacemaker can be programmed to a
fixed rate mode or a magnet can be placed over the generator to
temporarily convert the pacemaker to a fixed rate mode. Pace-
makers with sensing capabilities (VVI, DDD pacemakers) are
temporarily converted to a fixed rate (V00, D00) mode when a
magnet is placed over a pacemaker generator.
Endless loop or pacemaker-mediated tachycardia can occur
with DDD pacing as well as with other modes of pacing such
as VDD, VAT, and DDT. The tachycardia can be terminated
by reprogramming the pacemaker to other modes such as
VVI or DVI or a magnet can be applied to the pacemaker
generator, temporarily converting the pacemaker to a fixed
rate or D00 mode. If the pacemaker needs to remain in DDD
mode, the pacemaker can be programmed not to recognize
the retrograde P wave by lengthening the refractory period of
the atrial channel.
Permanent pacemakers: The indications for insertion of
permanent pacemakers in patients with acquired AV block are
discussed in Chapter 8, Atrioventricular Block; for patients
with intraventricular conduction defect, in Chapter 11, Intra-
ventricular Conduction Defect: Trifascicular Block; and for
patients with sick sinus syndrome, in Chapter 12, Sinus Node
Dysfunction.
Whenever there is a need for a permanent pacemaker, two
other conditions should always be considered before the per-
manent pacemaker is implanted: the need for biventricular
pacemaker in patients with bundle branch block and the
need for ICD in patients with left ventricular dysfunction.
Biventricular pacemakers: Implantation of biventricular
pacemaker (also called cardiac resynchronization therapy),
is indicated in patients with a QRS duration of 0.12 sec-
onds, who have systolic left ventricular dysfunction (ejec-
tion fraction 35%) and continue to have symptoms of
heart failure (Class III or Class IV) in spite of optimal med-
ical therapy for heart failure. Cardiac resynchronization is
performed by pacing both ventricles simultaneously. Si-
multaneous pacing of both ventricles will significantly de-
crease the delay in the spread of electrical impulse to both
ventricles when there is bundle branch block. Biventricular
pacing has been shown to improve cardiac output in patients
with wide QRS complexes. The patient should be in normal
LWBK271-C26_414-434.qxd 29/1/09 9:42 pm Page 433 LWBK270-4119G-C02_073-110.qxd
sinus rhythm so that timing of atrial and ventricular con-
traction can be synchronized. Although most patients who
have received biventricular pacemakers have left bundle
branch block, currently, the width of the QRS complex
rather than the type of bundle branch block is the main in-
dication for biventricular pacing.
Implantable cardioverter defibrillators: Patients with
severe left ventricular dysfunction are at risk for sudden
cardiac death due to ventricular tachycardia or ventricu-
lar fibrillation. These patients therefore are also candi-
dates for implantation of ICD.
n Secondary prevention: ICD may be implanted for
secondary prevention of sudden cardiac death imply-
ing that these patients have experienced and survived
a previous episode of cardiac arrest or sustained ven-
tricular tachycardia.
n Primary prevention: These patients have not experi-
enced any previous arrhythmias or cardiac arrest but
are high risk for ventricular tachycardia or ventricular
fibrillation. For primary prevention of sudden cardiac
death, the following are Class I indications for implan-
tation of ICD according to the American College of
Cardiology/American Heart Association/Heart Rhythm
Society 2008 guidelines for device-based therapy of
cardiac rhythm abnormalities.
n Left ventricular ejection fraction 35% due to
prior myocardial infarction (MI) who are at least
40 days post-MI and are in New York Heart
Association (NYHA) functional Class II or III.
n Nonischemic dialated cardiomyopathy with ejec-
tion fraction 35% and who are in NYHA func-
tional Class II or III.
n The following are Class IIa recommendations for
primary prevention of sudden cardiac death.
n Left ventricular dysfunction due to prior MI who
are at least 40 days post-MI, have an ejection frac-
tion 30% and are in NYHA functional Class I.
n Selected patients with idiopathic hypertrophic
subaortic stenosis who have 1 or more major risk
factors for sudden cardiac death. This includes
strong family history of sudden cardiac death, ab-
normal blood pressure response during exercise
testing, unusually thick ventricular septum 3.0
cm, and spontaneous nonsustained VT or unex-
plained syncope.
The ECG of Cardiac Pacemakers 433
n Patients with arrhythmogenic right ventricular
dysplasia or cardiomyopathy who have 1 or more
risk factors for sudden cardiac death. This includes
male gender, severe right ventricular (RV) dilata-
tion and extensive RV involvement, LV involve-
ment, young age (5 years) and nonsustained
ventricular tachycardia during monitoring or in-
duction of ventricular tachycardia during electro-
physiologic testing.
Similar to pacemakers, ICDs may be affected by electromag-
netic interferences including those emitted by electronic arti-
cle surveillance system, which are deployed as antitheft de-
vices in shopping centers. This may cause the ICD to
discharge inappropriately if the patient is exposed long
enough to the effects of the antitheft device.
Suggested Readings
Bernstein AD, Camm AJ, Fletcher RD, et al. NASPE/BPEG
generic pacemaker code for antibradyarrhythmia and adaptive-
rate pacing and antitachyarrhythmia devices. Pacing Clin
Electrophysiol. 1987;10:794799.
Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm
abnormalities: a report of the American College of Cardiol-
ogy/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Revise the ACC/AHA/
NASPE 2002 Guideline Update for Implantation of Cardiac
Pacemakers and Antiarrhythmia Devices). Circulation. 2008;
117:e350e408.
Gimbel JR, Cox Jr, JW. Electronic article surveillance systems
and interactions with implantable cardiac devices: risk of ad-
verse interactions in public and commercial spaces. Mayo
Clin Proc. 2007;82:318322.
Hayes DL. Pacemakers. In: Topol EJ, ed. Textbook of Cardiovas-
cular Medicine. 2nd ed. Philadelphia: Lippincott Williams &
Wilkins; 2002:15711596.
Mower MM, Aranaga CE, Tabatznik B. Unusual patterns of con-
duction produced by pacemaker stimuli. Am Heart J. 1967;
74:2430.
Parsonnet V, Furman S, Smyth PD. A revised code for pace-
maker identification. Pacemaker Study Group. Circulation.
1981;64:60A62A.
Surawicz B, Uhley H, Borun R, et al. Task Force I: standardiza-
tion of terminology and interpretation. Am J Cardiol.
1978;41:130144.
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Commonly Used Injectable
Pharmacologic Agents
Adenosine (Adenocard): Pregnancy
Category C
Indication: Drug of choice for the conversion of
paroxysmal supraventricular tachycardia (PSVT) to
normal sinus rhythm.
Mechanism of action: Adenosine is an atrioventricu-
lar (AV) nodal blocker and can interrupt supraventric-
ular arrhythmias that are AV nodedependent. It also
inhibits the sinus node resulting in depression of sinus
node function.
Intravenous dose:
Rapid bolus of 6 mg given intravenously as quickly as
possible (within 1 to 2 seconds) preferably to a proxi-
mal vein. The injection should be followed by a flush
of 10 to 20 mL normal saline using a separate syringe.
To enhance delivery of the pharmacologic agent to
the heart, the arm should be elevated immediately af-
ter the injection especially if a distal vein is used.
If the supraventricular tachycardia (SVT) is not
converted after 1 to 2 minutes, a higher dose of 12
mg is given.
If the SVT has not converted, a third and final dose
of 12 mg is given.
A rhythm strip should always be recorded during in-
jection, which may be useful in the diagnosis of other
tachycardias other than paroxysmal SVT (PSVT).
Contraindications:
Adenosine can cause bronchoconstriction in pa-
tients with asthma or in patients with history of
bronchospastic pulmonary disease.
Patients with sick sinus syndrome may develop pro-
nounced bradycardia after the PSVT is terminated.
Other things you should know about adenosine:
Intravenous doses of more than 12 mg are not rec-
ommended.
Injection into a central IV line may result in a more
pronounced effect. Consider giving a smaller initial
dose of 3 mg if adenosine is injected into a central line.
Appendix
Carbamazepine and dipyridamole potentiate the ef-
fects of adenosine. If the patient is on any of these
agents, the initial dose of adenosine should also be
reduced to 3 mg.
Methylxanthines such as caffeine and theophylline
is the antidote of adenosine. The usual dose of
adenosine may not be effective in patients who are
on theophylline. Larger doses are necessary, but
should not be given if the patient is taking theo-
phylline for bronchospastic pulmonary disease.
Sixty percent of patients with PSVT will convert to
normal sinus rhythm within 1 minute after an initial
bolus of 6 mg and up to 92% after a 12-mg bolus.
The elimination half-life of adenosine is 10 seconds.
Transient periods of asystole, AV block, or bradycardia
frequently occur before conversion to normal sinus
rhythm. The antidote for adenosine is aminophylline
given intravenously. The antidote is rarely needed be-
cause the half-life of adenosine is very short.
When given to patients with wide complex tachycar-
dia, adenosine can depress left ventricular function,
but because of its short half-life, its effect is transient
and is usually tolerable even in patients with poor left
ventricular dysfunction. It receives a Class IIb recom-
mendation by the American College of Cardiology/
American Heart Association/European Society of
Cardiology guidelines on supraventricular arrhyth-
mias when given to patients with wide complex
tachycardia of unknown origin.
Adenosine should be used cautiously in patients
with severe coronary artery disease because adeno-
sine is a potent coronary vasodilator and can cause
ischemia by redistributing coronary flow to normal
vessels.
Prolonged asystole, ventricular tachycardia, and
ventricular fibrillation may occur.
Atrial fibrillation can occur in up to 10% of patients
and may be catastrophic in a patient with Wolff-
Parkinson-White (WPW) syndrome.
Adenosine does not convert atrial flutter or atrial
fibrillation to normal sinus rhythm but can slow
435
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436 Appendix
ventricular rate transiently, which may be useful if
the diagnosis of the narrow complex tachycardia is
uncertain.
Amiodarone (Cordarone): Pregnancy
Category D
Indication: Amiodarone is indicated only for the
treatment of ventricular arrhythmias. The use of amio-
darone in the treatment of supraventricular arrhyth-
mias and control of ventricular rate in atrial flutter or
fibrillation is not recommended by the Food and Drug
Administration (FDA) and its use is based solely on
published information.
Ventricular arrhythmias:
n Amiodarone IV is indicated for the treatment of
ventricular tachycardia (VT) in patients with
normal left ventricular systolic function and in
patients with systolic dysfunction.
n It is also indicated for the treatment of ventricu-
lar fibrillation (VF) and pulseless VT.
n Indicated for the treatment of wide complex
tachycardia of uncertain etiology.
Supraventricular arrhythmias:
n Accepted as a second- or third-line agent for the
termination of atrial tachycardia from enhanced
automaticity including focal atrial tachycardia,
multifocal atrial tachycardia, and other types of
atrial tachycardia resulting from reentry that are
refractory to medical therapy.
n Although amiodarone is extensively used and is
effective in controlling the ventricular rate in atrial
fibrillation and converting patients with atrial fib-
rillation to normal sinus rhythm, it has not been
approved by the FDA for these indications.
Mechanism of action: Amiodarone is generally a
Class III antiarrhythmic agent, but exhibits all Class I
to IV properties of the Vaughan Williams classification.
Thus, similar to Class I agents, it is a sodium channel
blocker; similar to beta blockers (Class II), it has anti-
sympathetic properties; and similar to Class III agents,
it blocks the potassium channel and therefore prolongs
the duration of the action potential, slows conduction
and prolongs the refractory period. It also has Class IV
negative chronotropic effects on AV nodal tissues simi-
lar to calcium blockers thereby slowing AV conduction.
Intravenous dose:
Sustained VT or wide complex tachycardia of
unknown origin:
n Initial bolus: 150 mg given IV rapidly for 10
minutes (150 mg or 3 mL of amiodarone is di-
luted with 100 mL D5W and infused over 10
minutes equivalent to 15 mg/minute).
n This infusion may be repeated every 10 minutes
as needed.
Cardiac arrest from pulseless VT or VF:
n Initial bolus: Amiodarone is given at a bigger
dose of 300 mg diluted to 20 to 30 mL of saline
or D5W given IV push.
n This may be followed by supplementary boluses of
150 mg IV given by IV push every 3 to 5 minutes.
Next 6 hours: Follow initial bolus with an IV drip of
1 mg/minute  6 hours (total  360 mg). The solu-
tion is prepared by adding 900 mg of 18 mL of amio-
darone to 500 mL D5W (or 450 mg in 250 mL D5W).
n If the arrhythmia keeps recurring, an alternative
is to give the solution as 150 mg IV boluses for 10
minutes every 10 to 15 minutes as needed, in-
stead of giving the solution by IV drip.
Next 18 hours: Continue the IV drip to a lower
dose of 0.5 mg/minute  18 hours (total  540 mg).
The maximum total cumulative dose including dose
used in resuscitation should not exceed 2.2 g in the
first 24 hours.
After 24 hours: The intravenous dose is main-
tained after 24 hours:
n The infusion is continued at 0.5 mg/minute  24
hours. Maintenance infusion of 0.5 mg/minute
can be continued for several days and if neces-
sary up to 2 to 3 weeks.
n If patient develops recurrence of the ventricular
arrhythmia at any time during infusion, a sup-
plemental bolus of 150 mg diluted with 100 mL
D5W may be given IV over 10 minutes.
n The maximum daily dose should not exceed
2,100 mg. Intravenous dosing should be switched
to oral medication when the arrhythmia has
been suppressed.
n Doses 2,200 mg/24 hours are associated with
significant hypotension.
Other things you should know about amio-
darone:
Amiodarone is the preferred drug for ventricular ar-
rhythmias and some atrial arrhythmias when there is
left ventricular systolic dysfunction (ejection fraction
40% or when congestive heart failure is present).
Amiodarone is indicated only for the treatment of
VT/VF but is also effective in the following conditions:
n It is effective in persistent VT or VF after defibril-
lation.
n It is effective in stable monomorphic VT.
n It is indicated for wide complex tachycardia that
has not been diagnosed to be either VT or wide
complex SVT.
n It is effective in regular polymorphic VT (no QT
prolongation).
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n It can be used as second- to third-line therapy for
conversion of SVT to normal sinus rhythm when
other drugs are not effective.
n It is effective in conversion of atrial fibrillation to
normal sinus rhythm.
n It is also effective in controlling ventricular rate
in atrial fibrillation especially in patients with
WPW syndrome.
Amiodarone prolongs the QTc and is proarrhythmic.
Its proarrhythmic effect however is much less than
the other antiarrhythmic agents. It should not be ad-
ministered with other agents that prolong the QTc.
The half-life of intravenous boluses varies from 4.8
to 68 hours and becomes longer as tissues become
saturated. After steady state is reached, amiodarone
has a long and variable half-life from 40 days to 3 to
5 months.
It can cause multiple organ toxicity including hepa-
tocellular damage, hyper- or hypothyroidism, optic
neuritis, and pulmonary disorders including acute
respiratory distress syndrome.
Acute hepatocellular injury may occur with doses
that are larger than recommended.
Its hypotensive and bradycardic effects are fre-
quently related to the rapidity of infusion rather
than the dose.
It is metabolized through the cytochrome P450
(CYP 450) 3A4 and 2C9 pathways and therefore has
the potential for several drug-drug interactions.
n Statins (lovastatin, atorvastatin, and simvastatin
but not pravastatin or rosuvastatin) are metabo-
lized through the CYP 450 3A4 pathway. Serum
concentration of these statins can increase result-
ing in higher incidence of myopathy or rhab-
domyolysis.
n Calcium channel blockers such as verapamil and
diltiazem are also metabolized through the CYP
450 3A4 pathway. The effects of these agents can
be potentiated by amiodarone resulting in signif-
icant bradycardia.
n CYP 450 3A4 inhibitors such as grapefruit juice,
protease inhibitors, and cimetidine may increase
the serum levels of amiodarone and can poten-
tially cause amiodarone toxicity.
n Agents that accelerate the CYP 450 3A4 meta-
bolic pathway such as rifampin, barbiturates, and
St. Johns wort may decrease the blood levels of
amiodarone making it subtherapeutic.
n Amiodarone is also metabolized through the
CYP 450 2C9 pathway and therefore competes
with the metabolism of warfarin resulting in
prolongation of the prothrombin time. The
maintenance dose of warfarin should be reduced
when amiodarone is started. Patients on warfarin
Commonly Used Injectable Pharmacologic Agents 437
should have prothrombin tests monitored care-
fully.
n Beta blockers in combination with amiodarone
can cause profound bradycardia.
n Amiodarone can also potentiate the effect of dig-
italis; hence, the maintenance dose of digoxin
should be reduced by half when amiodarone is
given.
n Effective plasma concentration of amiodarone is
between 1 to 2 mcg/mL. The plasma concentra-
tion of amiodarone may be helpful in monitor-
ing the efficacy but not toxicity. The effective
therapeutic levels of amiodarone overlap with
toxic levels and should not exceed 3 to 4 mcg/L.
Atenolol (Tenormin): Pregnancy
Category D
Indication: Atenolol is indicated in the management
of patients with angina pectoris, acute myocardial in-
farction, and control of hypertension. Although
atenolol does not carry indication for termination of
SVT or for controlling the ventricular rate in atrial flut-
ter or fibrillation, it is frequently used for this purpose
based on published information.
Mechanism of action: Atenolol is a synthetic selective
1 adrenergic blocking agent. When given in high doses,
1 receptor blocking agents including atenolol are not
specific 1 blockers but also blocks 2 receptors, which
are present in bronchial and vascular smooth muscles.
Dose: The IV dose of atenolol for patients with acute
myocardial infarction (or for the management of
supraventricular arrhythmias), is 5 mg IV given slowly
over 5 minutes. Injection rate should not exceed 1
mg/minute. A second dose of 5 mg is given IV after 10
minutes if the first dose was well tolerated. The blood
pressure, heart rate, and electrocardiogram should be
monitored during the intravenous infusion. If the in-
travenous dose is well tolerated, an oral dose of 50 mg
is given 10 minutes after the last IV dose followed by
another 50 mg 12 hours later. The maintenance dose is
50 mg twice daily or 100 mg once daily.
Other things you should know about atenolol:
Unlike metoprolol or propranolol, atenolol is pri-
marily excreted by the kidneys (85%) and is not me-
tabolized or is only minimally metabolized by the
liver. Thus, atenolol given orally does not undergo
first pass degradation by the liver. When there is re-
nal failure, the dose should be adjusted.
When atenolol is given orally, only approximately
50% is absorbed. The other half is excreted un-
changed in the gastrointestinal tract. This is unlike
metoprolol where absorption is rapid and complete
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438 Appendix
when given orally. Metoprolol is primarily metabo-
lized in the liver and 50% of the oral dose is elimi-
nated during first pass.
The elimination half-life of atenolol is approxi-
mately 7 hours, but is much longer when there is re-
nal dysfunction.
Abrupt discontinuation or cessation of any beta
blocker, including atenolol, in patients with known
coronary disease and symptoms of angina may re-
sult in exacerbation of anginal symptoms or occur-
rence of acute coronary syndrome.
The latest 2007 focused update of the American Col-
lege of Cardiology/American Heart Association 2004
guidelines raises doubt about the safety of intra-
venous beta blockers in acute ST elevation myocar-
dial infarction and should not be given to patients at
increased risk for cardiogenic shock (see Metoprolol).
Atenolol is the only beta blocker that receives a cate-
gory D pregnancy risk classification by the FDA. All
other beta blockers receive a category C classifica-
tion. Sotalol, which also has beta blocking proper-
ties, carry a category B classification.
Atropine Sulfate: Pregnancy Category C
Indication: According to the 2005 American Heart As-
sociation guidelines for cardiopulmonary resuscitation
and emergency cardiovascular care, atropine remains
the first-line drug for the treatment of acute sympto-
matic bradycardia. It is indicated for the treatment of
acute symptomatic bradyarrhythmia due to sinus node
dysfunction, AV nodal block, and increased vagal activ-
ity. It is the second drug of choice after epinephrine or
vasopressin, in patients with ventricular asystole and
pulseless electrical activity.
Mechanism of action: Atropine is an anticholinergic
agent and increases ventricular rate by reversing vagally
mediated mechanisms of bradycardia and hypotension.
Dosing:
Asystole: For asystole or slow pulseless electrical ac-
tivity, a dose of 1.0 mg is given IV. If not effective, the
dose is repeated every 3 to 5 minutes until a maxi-
mum dose of 3.0 mg is given. Complete vagal block-
ade occurs at a total dose of 0.04 mg/kg, which is 2.0
mg for a 50-kg and almost 3.0 mg for a 70-kg patient.
Bradycardia from AV block or sinus dysfunc-
tion: The initial dose is 0.5 to 1.0 mg IV every 3 to
5 minutes as needed until the maximum dose is given.
Other things you should know about atropine:
For the treatment of bradycardia, doses of 0.5 mg
should not be given because small doses of atropine
can cause paradoxical slowing of the heart rate.
Small doses of atropine are parasympathomimetic.
It stimulates the vagal nuclei, resulting in paradoxi-
cal slowing. This paradoxical effect can also occur if
injected subcutaneously or intramuscularly. At-
ropine should always be given IV. If an IV route is
not available during cardiac resuscitation, it can be
given intratracheally at a dose of 2 to 3 mg diluted
with 10 mL normal saline.
It is not effective and should not be given to patients
with infranodal blocks (AV block below the level of
the AV node) such as those due to Mobitz II second-
degree AV block and complete AV block below the
level of the AV node with wide QRS escape com-
plexes (Class IIb recommendation).
Should be avoided in patients with bradycardia
from hypothermia.
The use of atropine should not delay the insertion of
transcutaneous or transvenous pacing in patients
with symptomatic bradycardia with low cardiac
output.
Beta Blockers: Beta Blockers are
Class II Agents According to the
Vaughan Williams Classification of
Anti-Arrhythmic Agents
Beta blockers that are available intravenously include
atenolol, esmolol, metoprolol, and propranolol. These
different beta blockers are discussed individually in al-
phabetical listing.
Digoxin (Lanoxin): Pregnancy
Category C
Indication: Control of ventricular rate in atrial fibril-
lation. It is also used for control of ventricular rate in
atrial flutter and conversion of PSVT to normal sinus
rhythm although these two indications have not been
approved by the FDA.
Mechanism of action:
Digoxin inhibits sodium-potassium ATPase, which
is an enzyme that regulates the exchange of sodium
and potassium inside the cells. When ATPase is in-
hibited, sodium builds up within the cells. Sodium
buildup activates the sodium-calcium exchange
mechanism. Increase in calcium inside the cell acti-
vates the intracellular cytosol system to release more
calcium. The increased calcium inside the cell en-
hances myocardial inotropicity with increased my-
ocardial systolic contraction.
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Commonly Used Injectable Pharmacologic Agents
Digoxin also affects the cardiovascular system indi-
rectly by its effect on the autonomic nervous system.
n It has parasympathetic effects, which inhibits the
sinus node, thus slowing the heart rate and slow-
ing conduction at the AV node.
n It reduces activity of the sympathetic nervous
system and renin-angiotensin-aldosterone-system,
thus reducing the activation of the neurohor-
monal system. This is mediated through barore-
ceptors sensitization, which causes increased
afferent inhibitory activities.
Intravenous dose:
Before giving a full loading dose, first ascertain that
the patient is not already on digoxin.
The ideal serum therapeutic level of digoxin is 0.7 to 1.1
ng/mL. The dose of digoxin that is needed to achieve
this level in a 70-kg man is 0.6 to 1.0 mg (10 to 15
mcg/kg). The total dose depends on the lean body mass
(and not total body weight) and renal function. Fifty
percent of the total dose is given initially. Subsequent
additional doses are given at 6- to 8-hour intervals.
Thus, if the patient weighs 70 kg, the total digitaliz-
ing dose is approximately 1.0 mg. Half the total dose
or 0.5 mg, is given IV followed by another 0.25 mg
IV in 6 hours and 0.25 mg IV after another 6 hours.
The patient will have received the full digitalizing
dose of 1.0 mg in 12 hours.
Digoxin is excreted primarily in the kidneys. Renal
excretion is dependent on glomerular filtration. In
patients with renal dysfunction, the creatinine clear-
ance should be calculated using the Cockroft and
Gault formula: Creatinine clearance for men  {(140
age)  (weight in kg)} divided by 72  serum crea-
tinine (in mg/mL). The calculated renal clearance
for men is multiplied by 0.85 for women.
n If the creatinine clearance is 90, the normal
dosage is unchanged.
n If the creatinine clearance is 60 to 89, mainte-
nance dose is 0.125 mg daily.
n If the creatinine clearance is 30 to 59, 0.125 mg is
given every other day.
n If the creatinine clearance is 29, use digoxin
very cautiously.
Other things you should know about digoxin:
Intramuscular injection of digoxin is very painful.
Parenteral injections therefore should be limited in-
travenously.
Rapid injection or infusion can cause systemic and
coronary constriction. Injection of digoxin there-
fore should be given slowly over 5 minutes or longer
and not given as a bolus injection.
Serum concentrations of digoxin are not altered sig-
nificantly by increase in body fat, thus lean body
439
weight and not total body weight correlates best
with the distribution space of digoxin.
The half-life of digoxin in patients with normal kid-
ney function is 1.5 to 2 days. In anuric patients, it is
prolonged to 3.5 to 5 days. Maintenance dosing can
be given once per day.
Elderly patients, especially those with renal dysfunc-
tion, may be difficult to digitalize because mainte-
nance dosing may be difficult; hence, serum digoxin
level should be monitored.
When assessing for serum digoxin level, blood
should be drawn after steady state is reached to allow
proper equilibration between serum and tissue lev-
els. Therefore, the level should be assayed just before
the next daily dose. If not possible, at least 6 to 8
hours after the last dose should have elapsed regard-
less whether oral or IV preparation is being given.
The serum level will be 10% to 25% lower after 24
hours as compared with 8 hours with once-daily
dosing, but minor differences in serum level with
twice-daily dosing at 8 or 12 hours after last dose.
The initial high levels of digoxin do not reflect the
actual concentration at the site of action until a
steady state of distribution occurs during chronic
use. Serum level reflects pharmacologic effect when
serum concentrations are in equilibrium with tissue
concentrations.
The serum level of digoxin should not exceed 1.3
ng/mL. Higher levels may be necessary to control
the ventricular rate in atrial fibrillation as compared
with digoxin being given for inotropic support in
heart failure; nevertheless, higher serum digoxin
levels were associated with a higher mortality in the
Digitalis Investigation Group study.
Digoxin competes with amiodarone and quinidine.
These two drugs are the most significant in increas-
ing the digoxin levels. Therefore, the dose of digoxin
should generally be halved when giving digoxin in
combination with these drugs. Digoxin level should
be monitored.
Digitalis has a tendency to increase automaticity
and at the same time cause AV block; thus, auto-
matic atrial tachycardia with 2:1 AV block is usually
a manifestation of digitalis toxicity. Other arrhyth-
mias associated with digitalis include ventricular ec-
topy, bidirectional ventricular tachycardia, sinus
dysfunction, and all degrees of AV block.
Digoxin is not removed by dialysis; therefore, dialy-
sis or exchange transfusion is not effective in treat-
ing digitalis toxicity. Most of the drug is bound to
tissue and does not circulate freely.
Digibind is the antidote for digitalis toxicity. This is
given intravenously and the dose is calculated ac-
cording to the serum digoxin level. Digibind should
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440 Appendix
be given only for life-threatening arrhythmias such
as paroxysmal atrial tachycardia with block or sig-
nificant bradyarrhythmias from AV block or sinus
dysfunction.
Digibind is excreted by the kidneys as a digoxin-
Digibind complex. When there is renal failure, the
Digibind-digoxin complex may not be excreted or
excretion may be significantly delayed. Thus, digi-
talis toxicity may recur after 72 hours because the
effect of Digibind in binding be effective after that
time.
The serum level of digoxin does not reflect the
digoxin level after Digibind is given. Thus it is not
possible to reassess digoxin toxicity after the antidote
is given.
Slowing of the ventricular rate in patients with heart
failure is more pronounce when digoxin is com-
bined with a beta blocker (such as carvedilol) com-
pared with the use of either drug alone.
Avoid electrical cardioversion if patient is on
digoxin. If cardioversion is necessary, use lower cur-
rent during cardioversion.
Diltiazem (Cardizem Injectable or
Lyo-Jet Syringe): Pregnancy Category C
Indication: Conversion of paroxysmal supraventricu-
lar tachycardia to normal sinus rhythm, control of ven-
tricular rate in atrial flutter, or fibrillation or in patients
with multifocal atrial tachycardia.
Mechanism of action: Diltiazem, like verapamil, is a
nondihydropyridine calcium channel blocker. It in-
creases refractoriness of the AV node and can slow
down the rate of the sinus node. It is a negative in-
otropic agent and can decrease myocardial contractil-
ity. It relaxes vascular smooth muscle resulting in peri-
pheral vasodilatation.
Intravenous dose:
Initial bolus of 0.25 mg/kg (approximately 15 to 20
mg for a 70-kg patient) given slowly IV over 2 min-
proper-
utes. If not effective, a second dose of 0.35 mg/kg
(approximately 20 to 25 mg for a 70-kg patient) may
be given after 15 minutes, slowly, IV. The heart rate
and blood pressure should be monitored during IV
infusion.
To prolong the half-life of diltiazem and maintain
control of ventricular rate in atrial fibrillation, an
intravenous drip of 5 to 15 mg/hour should be
started after giving the intravenous bolus.
Additional small boluses of 5 mg may be given in-
termittently during infusion if ventricular rate is not
optimally controlled with maintenance IV infusion.
Other things you should know about diltiazem:
Diltiazem is just as effective as verapamil in convert-
ing PSVT to normal sinus rhythm, but is less nega-
tively inotropic and may be used cautiously in pa-
tients with left ventricular dysfunction who are not
hemodynamically decompensated.
The elimination half life of IV diltiazem is approxi-
mately 3 to 5 hours and is shorter than verapamil.
Because of the relatively short half-life, a mainte-
nance infusion is necessary when controlling the
heart rate in atrial fibrillation. The maintenance in-
fusion dose is 5 to 15 mg/hour. While on mainte-
nance infusion, an oral dose should be started
within 3 hours after the initial IV dose so that the in-
fusion can be discontinued within 24 hours unless
the patient can not take oral medications.
Although IV diltiazem may be tolerable in patients
with atrial arrhythmias with mild heart failure,
they should not be given to patients with acutely
decompensated heart failure. Oral nondihydropy-
ridine calcium channel blockers, including oral
diltiazem, should not be given when there is left
ventricular dysfunction. It should not be given for
wide complex tachycardia of unknown origin, sick
sinus syndrome, or atrial fibrillation associated
with WPW syndrome.
Severe bradycardia and hypotension may occur
when diltiazem is combined with beta blockers.
Dobutamine (Dobutrex): Pregnancy
Category B
Indication: Dobutamine is indicated for the treat-
ment of heart failure. It is also used off-label for the
treatment of bradyarrhythmias and heart block not
responsive to atropine, especially in treatment of in-
franodal AV block.
Mechanism of action: Dobutamine is a synthetic cat-
echolamine with predominantly 1 and slight 2
adrenergic properties and mild to moderate
ties.
Dosing: Given as IV infusion with an initial dose of
1 mcg/kg/minute and increased to 2.5 to 5.0 mcg/
kg/minute. This can be titrated gradually every 3 min-
utes according to heart rate to a maximum dose of 20
mcg/kg/minute. Higher doses up to 40 mcg/kg/minute
can be given but are usually associated with atrial and
ventricular arrhythmias. The use of dobutamine for AV
block and bradyarrhythmias should only be tempo-
rary, before a temporary pacemaker can be inserted.
The drug very often comes in premix infusion of 500
mg in 250 mL D5W.
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Other things you should know about dobutamine:
Dobutamine has a short elimination half-life of 2
minutes and should be given as a continuous intra-
venous infusion.
It is indicated for the treatment of patients with low
cardiac output or heart failure. It is also used off-label
as temporary measure for treatment of sympto-
matic bradyarrhythmia before a pacemaker can be
inserted. It is the preferred agent in infranodal AV
block with wide escape complexes, because atropine
is not effective when AV block is infranodal. It can
also be tried in patients with symptomatic brad-
yarrhythmias not responsive to atropine before a
pacemaker can be inserted.
The chronotropic effect of dobutamine is not as po-
tent as dopamine or isoproterenol and is more often
used as an inotropic agent in acute heart failure
rather than for its chronotropic effect in patients
with bradyarrhythmias or AV block. If dobutamine
is not effective in increasing the heart rate, isopro-
terenol should be given instead.
Epinephrine: Pregnancy Category C
Indication: Epinephrine is indicated for cardiac arrest
due to VF or pulseless VT. It is also indicated for the
treatment of anaphylaxis and syncope from complete
heart block or hypersensitive carotid sinus and for the
treatment of asthma.
Mechanism of action: The drug is a sympath-
omimetic catecholamine with
-, 1-, and 2-adrener- give a second bolus of 0.5 mg/kg over 1 minute and
gic activity. It has the most potent
-adrenergic effect increase infusion rate by 50 mcg for an infusion rate
resulting in intense vasoconstriction, which can result
in coronary and cerebral perfusion pressure during
cardiopulmonary resuscitation. It is this intense
- If not effective, give a third and final bolus of 0.5 mg/kg
adrenergic effect that is useful in cardiac arrest.
Dose: According to the 2005 American Heart Associa-
tion guidelines for cardiopulmonary resuscitation, the
dose of epinephrine in cardiac resuscitation is 1 mg
given by intravenous or if not possible by intraosseous
administration every 3 to 5 minutes. Higher doses may
be given to overcome beta blocker or calcium channel
overdose. If intravenous or intraosseous administra-
tion is not possible during resuscitation, it may be
given intratracheally at a dose of 2 to 2.5 mg. Higher
doses of epinephrine has not been shown to be more
effective than standard doses during cardiopulmonary
resuscitation.
For anaphylaxis, the drug is given intramuscularly
0.3 mg, which may be repeated if needed. It may also
be given subcutaneously at a dose of 0.2 to 1.0 mg.
For asthma, the drug is given subcutaneously 0.2 to
0.5 mg. If needed for severe attacks, a second and
Commonly Used Injectable Pharmacologic Agents 441
third dose may be given every 20 minutes for a max-
imum of three doses.
Esmolol (Brevibloc): Pregnancy
Category C
Indication: Esmolol is indicated for the conversion of
SVT to normal sinus rhythm and control of ventricular
rate in patients with atrial fibrillation or atrial flutter. Also
indicated for the treatment of inappropriate, noncom-
pensatory sinus tachycardia and hypertension that occur
during induction and tracheal intubation, during surgery
or emergence from anesthesia and postoperative period.
Mechanism of action: Esmolol is a selective 1
blocker.
Dose: The dose of esmolol is quite complicated
because the drug is very short acting and may need
frequent retitration:
The initial IV loading dose is 0.5 mg/kg over 1
minute followed by an infusion of 50 mcg/kg/
minute for 4 minutes. If effective, the infusion rate is
continued. The dose can be titrated depending on
the desired ventricular rate during atrial flutter or
fibrillation. Thus, the maintenance infusion rate can
be increased from 50 to 100 mcg/kg/minute, and
after 4 or more minutes to 150 mcg/kg/minute and
subsequently up to a maximum of 200 mcg/kg/
minute.
If the first bolus is not effective, another option is to
of 100 mcg/kg/minute for 4 minutes. If effective,
continue the infusion rate.
over 1 minute and increase infusion rate by 50 mcg for
an infusion rate of 150 mcg/kg/minute for 4 minutes.
The infusion rate can be increased by 50 mcg/kg/
minute to a maximum of 200 mcg/kg/minute.
The usual maintenance infusion rate is 50 to 200
mcg/kg/minute. Maintenance infusion can be given
for 24 hours if necessary; however, the patient should
be monitored for hypotension and bradycardia.
A higher maximum maintenance infusion dose of
50 to 300 mcg/kg/minute may be given for the treat-
ment of hypertension.
Other things you should know about esmolol:
Esmolol has a very short half-life of only 2 to 9 min-
utes. The drug is too short-acting, making routine
use for control of ventricular rate in atrial flutter
and fibrillation difficult to maintain in the medical
intensive care unit, more especially when long-term
control is necessary. The short half-life, however,
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442 Appendix
may be advantageous to patients who develop ar-
rhythmia during the perioperative and immediate
postoperative period where immediate and short-
term control is all that is needed.
Esmolol is also indicated for hypertension occurring
during the perioperative and immediate postopera-
tive period. For control of hypertension, a higher
maintenance infusion dose of up to 250 to 300 mcg/
kg/minute may be necessary (see dosing). It can also
be given as treatment for noncompensatory sinus
tachycardia, which, according to the judgment of
the physician, may be inappropriate and needs to be
controlled.
Dosing is not affected by hepatic or renal disease.
Can cause slowing of the sinus node, thus the agent
should be given cautiously when there is history of
sick sinus syndrome or previous bradycardia.
The maximum infusion dose should not exceed 200
mcg/kg/minute and the agent may be continued as
an infusion up to 24 hours.
Ibutilide (Corvert): Pregnancy
Category C
Indication: Rapid conversion of atrial flutter or atrial
fibrillation to normal sinus rhythm
Mechanism of Action: Ibutilide is a Class III antiar-
rhythmic agent. Class III agents block the potassium
channel and therefore prolong the duration of the ac-
tion potential. Conduction is slowed and atrial and
ventricular refractoriness are prolonged. The effect of
ibutilide is different when compared to other Class III
agents because it prolongs the action potential dura-
tion by slowing the inward flow of sodium during re-
polarization in contrast to most type III agents, which
slow the outward flow of potassium.
Dosing:
Before converting atrial flutter or atrial fibrillation
to normal sinus rhythm with ibutilide, any patient
known to have the arrhythmia for more than
48 hours should first be adequately anticoagulated
for at least 3 weeks before attempting conversion to
normal sinus rhythm. However, if a more immedi-
ate cardioversion seems necessary, a transesophageal
echocardiogram should be performed to exclude
thrombi in the atria or left atrial appendage. Car-
dioversion may then be carried out under adequate
anticoagulation if no thrombi are demonstrated.
For patients weighing 60 kg, the dose of ibutilide
is 1 mg given intravenously for 10 minutes. For pa-
tients weighing 60 kg, the dose is 0.01 mg/kg or a
maximum of 0.6 mg. One mg of ibutilide is avail-
able as a 10-mL preparation and is injected at a rate
of 1 mL/minute. The 10-mL preparation (1 mg) can
be injected directly IV (10 minutes) without dilu-
tion. It could also be diluted to a larger volume of 50
mL and infused intravenously for 10 minutes.
If the arrhythmia has not converted 10 minutes after
injection, the same dose can be repeated with the
same rate of administration. There is a 50% to 70%
chance for atrial flutter and 30% to 50% chance for
atrial fibrillation to convert to normal sinus rhythm
almost immediately after the drug is administered.
If the arrhythmia has not converted after the second
dose, no further injections should be given.
For postcardiac surgery patients weighing 60 kg,
0.5 mg (0.005 mg/kg per dose) given as a single or
double dose, was effective for atrial fibrillation and
flutter.
Other things you should know about ibutilide:
Sustained polymorphic ventricular tachycardia
(PVT) requiring cardioversion can occur in approx-
imately 1.7% of patients receiving intravenous ibu-
tilide. This arrhythmia can be fatal if not immedi-
ately recognized. PVT may or may not be associated
with baseline QTc prolongation; the tachycardia is
called torsades de pointes.
The initial episode of PVT can occur up to 40 min-
utes after initial infusion, although recurrence of
PVT can occur up to 3 hours after initial infusion.
Sustained PVT is more common in patients with
low ejection fraction or patients with history of con-
gestive heart failure, especially where there is base-
line QT prolongation. The drug, therefore, should
not be given to patients who are hemodynamically
unstable or in heart failure, in patients with recent
myocardial infarction or angina, patients with elec-
trolyte and blood gas abnormalities including pa-
tients with baseline QT prolongation, or those who
are metabolically deranged.
Nonsustained PVT occurred in an additional 2.7% of
patients and nonsustained monomorphic VT in 4.9%.
Cardiac monitoring should be continued for at least
4 hours after infusion or until QTc is back to baseline.
Longer monitoring is required for patients with he-
patic dysfunction. Prolongation of the QT interval is
related to the dose and infusion rate. Patients devel-
oping PVT should be monitored for a longer period.
The hemodynamic effect of the drug is similar in
patients with systolic dysfunction and those with-
out. No significant effect in cardiac output or pul-
monary wedge pressure has been noted. The drug
has not been shown to increase the duration of the
QRS complex.
When giving ibutilide, the QTc interval should
preferably be 440 milliseconds and the serum
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potassium at least 4.0 mEq/L. Patients with QTc
440 milliseconds and potassium 4.0 mEq/L
were not allowed to participate when clinical trials
with ibutilide were conducted.
Although torsade is the most common arrhythmia
associated with the drug, sinus arrest and complete
asystole can occur during conversion from atrial
flutter or atrial fibrillation to normal sinus rhythm
especially in patients with sick sinus syndrome.
The drug is more effective in atrial flutter than in
atrial fibrillation. Approximately 53% of patients
with atrial flutter will convert with the first 1 mg
dose and 70% after the second dose. In atrial fibril-
lation, approximately 22% will convert with the first
dose and 43% after the second dose. Conversion oc-
curred within 30 minutes after the start of infusion.
This is in contrast to intravenous sotalol (1.5
mg/kg), where only 18% of patients with atrial flut-
ter and 10% with atrial fibrillation converted during
clinical trials with the drug.
If atrial flutter or atrial fibrillation has not converted
after 90 minutes after the infusion is completed, the
patient can be electrically cardioverted if appropri-
ate. Other antiarrhythmic agents can also be started
4 hours after the infusion is completed.
Patients with more recent onset atrial flutter or
atrial fibrillation (within 30 days) have a higher
chance of conversion to normal sinus rhythm com-
pared with patients whose arrhythmias were of
longer duration. The efficacy of ibutilide has not
been tested in patients with atrial flutter or atrial fib-
rillation longer than 90 days in duration.
Isoproterenol (Isuprel): Pregnancy
Category C
Labetalol (Normodyne): Pregnancy
Indication: As a temporizing measure for the treat-
ment of heart block or symptomatic bradyarrhythmias
Category C
when atropine or dobutamine has failed. It is also given
as a temporizing measure for the treatment of torsades
de pointes before a pacemaker can be inserted.
Mechanism of Action: Isoproterenol is a -adrener-
gic agonist with very potent 1 and 2 properties.
Similar to other -adrenergic agents, it increases
1-, 1- and 2-adrenergic receptor blocking
cyclic AMP by stimulating adenyl cyclase, eventually
increasing intracellular calcium. It has very potent
chronotropic and inotropic properties and prevents
bronchospasm.
Dose: Given as an intravenous infusion at 2 to 10 mcg/
minute titrated according to the heart rate, It is usually
prepared by diluting 1 mg of isoproterenol to 500 mL
D5W, resulting in a concentration of 2 mcg/mL.
Commonly Used Injectable Pharmacologic Agents 443
Other things you should know about isopro-
terenol:
Isoproterenol is the drug of choice for the tempo-
rary treatment of infranodal AV block. It shortens
the refractory period of the AV node and enhances
AV conduction. It also increases automaticity allow-
ing latent pacemakers to become manifest. Because
of its serious side effects, it is potentially dangerous
to use routinely and should be used cautiously only
as a temporizing measure for the treatment of heart
block and bradyarrhythmias before a temporary
pacemaker can be inserted or after atropine or
dobutamine has failed.
Isoproterenol is a very potent 1- and 2-adrenergic
agent. It increases automaticity not only of the sinus
node but all cells with pacemaking potential, result-
ing in ectopic rhythms that may dominate over that
of the sinus node. It can cause ectopic atrial tachy-
cardia, atrial flutter, atrial fibrillation, and ventricu-
lar tachycardia or fibrillation even in patients with
structurally normal hearts.
Isoproterenol increases inotropicity and cardiac
output and markedly increases oxygen consump-
tion. It can provoke ischemia in patients with coro-
nary disease and can provoke arrhythmias especially
in patients with left ventricular dysfunction.
Torsades de pointes: Isoproterenol may be used as
a temporizing procedure in patients with bradycar-
dia dependent torsades de pointes before a tempo-
rary pacemaker can be inserted.
Isoproterenol should be given at the lowest dose
possible. Because it enhances myocardial oxygen
consumption, it can expand infarct size and
cause complex ventricular and supraventricular
arrhythmias.
Indication: Intravenous labetalol is indicated for the
emergency treatment of hypertension. It does not carry
indication for the treatment of cardiac arrhythmias.
Mechanism: Labetalol is a nonspecific beta blocker
with
properties. In addition, it also has intrinsic sympath-
omimetic activity.
Dose: For the treatment of hypertension, 10 mg is
given IV push over 1 to 2 minutes. The dose is re-
peated or doubled every 10 minutes if needed to a
maximum dose of 150 mg. Another option is to give
an initial bolus followed by an infusion of 2 to 8 mg/
minute.
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444 Appendix
Lidocaine (Xylocaine HCL): Pregnancy
Category B
Indication: For acute suppression of VT or VF.
Mechanism of Action: Lidocaine is Class IB antiar-
rhythmic agent. It blocks the sodium channel but has
no effect on potassium channel. It does not prolong
and may even shorten action potential duration and ef-
fective refractory period of the His-Purkinje system.
Dosing:
In cardiac arrest, an initial bolus of 1.0 to 1.5 mg/kg
is given. The higher dose is given only for ventricu-
lar fibrillation or pulseless VT after defibrillation
and epinephrine has failed.
For refractory VT or VF, an additional bolus of 0.5 to
0.75 mg/kg is given IV over 3 to 5 minutes. The rate
should not exceed 50 mg/minute. Lidocaine is distrib-
uted rapidly out of the plasma in 10 minutes. The
initial dose therefore is only transiently therapeutic
and additional boluses have to be given repeatedly
every 5 to 10 minutes, as needed, for a maximum total
loading dose of 3 mg/kg over 1 hour. The loading dose
should be decreased in patients with heart failure.
The initial loading dose is followed by an IV infusion of
1 to 4 mg/minute to maintain therapeutic blood levels.
Maintenance infusion should be adjusted to a lower
rate in patients with heart failure and liver disease.
The volume of distribution does not reach steady
state until after 8 to 10 hours or even longer, up to
24 hours in patients with liver disease, heart failure,
or low output states.
Other things you should know about lidocaine:
Lidocaine does not prolong action potential dura-
tion and therefore does not prolong the QT interval.
The drug is useful in patients with normal or pro-
longed QT intervals or patients with monomorphic
or polymorphic VT.
Is primarily indicated for patients with ischemic
VT/VF and is the drug of choice for VT/VF associ-
ated with acute myocardial infarction.
Unlike most antiarrhythmic agents, lidocaine can be
used in patients with impaired left ventricular function.
It is not effective in blocking the AV node and there-
fore is not useful in supraventricular arrhythmias. It
may even enhance AV conduction, which can result
in 1:1 AV conduction in atrial flutter.
Lidocaine as well as its metabolites undergoes
degradation through the CYP 450 3A4 pathway.
Continuous infusion of lidocaine at the same dose
for 24 to 48 hours increases its half-life and generally
leads to toxicity.
Symptoms of toxicity are usually from central nerv-
ous system involvement, which include seizures,
dysarthria or slurred speech, muscle twitching,
drowsiness, altered consciousness, or even coma.
Lidocaine should generally be discontinued 12
hours after the arrhythmia has been successfully
suppressed unless there is an indication to infuse the
medication for a longer period.
After the infusion is terminated, plasma levels slowly
decline over several hours. If the medication is no
longer needed, the medication can be discontinued
outright without tapering the dose.
Therapeutic blood levels can be monitored, which
ranges from 1.5 to 5 mcg/mL.
Magnesium Sulfate: Pregnancy
Category C
Indication: Replacement therapy in the presence of
magnesium deficiency. Also used in the treatment of
torsade de pointes characterized by polymorphous VT
with prolonged QT interval.
Mechanism of Action: Severe magnesium deficiency
can cause cardiac arrhythmias including ventricular
fibrillation and sudden cardiac death. Hypomagne-
semia also prevents the correction of potassium defi-
ciency.
Dosing:
For refractory VF: In emergent conditions where
there is refractory VF associated with magnesium
deficiency, dilute 1 to 2 g magnesium sulfate in 100
mL D5W and inject IV over 1 to 2 minutes.
For torsade: Even in the absence of magnesium de-
ficiency, give a loading dose of 1 to 2 g mixed with 50
to 100 mL D5W injected IV over 5 to 60 minutes, de-
pending on the urgency of administration. Follow
with a continuous IV infusion of 0.5 to 1.0 g/hour.
For magnesium deficiency: Dilute 5 g in 1 L D5W,
0.9% NaCl or lactated Ringers solution and given as
a continuous infusion. Maximum concentration is
4 g in 250 mL given IV over 3 hours. Dose should
not exceed a total of 30 to 40 g in adults and rate
should not exceed 50 mg/minute.
Metoprolol (Lopressor): Pregnancy
Category C
Indication: Metoprolol is indicated for reduction of
mortality in acute myocardial infarction. It is also indi-
cated for angina and hypertension. It is effective as an
antiarrhythmic agent in supraventricular arrhythmias
and reduces incidence of ventricular tachycardia/fibril-
lation in patients with acute myocardial infarction.
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Mechanism of action: Metoprolol is a cardioselective
1-adrenergic blocking agent.
Dose: The initial IV dose is 5 mg slowly over 5 min-
-adrenergic effect resulting in vasocon-
utes. May be repeated every 5 minutes if well tolerated
for a total of three doses or 15 mg over 15 minutes. If
maintenance oral dose is necessary and patient is post-
operative or NPO, give IV piggyback 20 mg over
2 hours. This is equal to 50 mg of oral metoprolol. The
IV dose is followed by an oral dose of 50 mg BID 
24 hours, then 100 mg BID.
Other things you should know about metoprolol:
The most recent 2007 focused update of the Ameri-
can College of Cardiology/American Heart Associa-
tion 2004 guidelines for the management of ST ele-
vation MI raises doubt about the safety of IV
metoprolol or similar beta blockers based on the re-
sults of a large clinical trial (Clopidogrel and Meto-
prolol in Myocardial Infarction). Although meto-
prolol IV has been shown to decrease reinfarction
and ventricular fibrillation in this study, there were
more episodes of cardiogenic shock. Thus, the use of
metoprolol IV is reasonable only when hyperten-
sion is present and the patient does not have any of
the following findings:
n Signs of heart failure
n Low output state
n Increased risk for cardiogenic shock (age 70
years, systolic blood pressure 120 mm Hg,
sinus tachycardia 100 beats per minute, or
heart rate 60 beats per minute and increased
time since onset of acute MI).
n Contraindications to beta blockade (PR 0.24
second, second- or third-degree AV block, reac-
tive airway disease or active asthma).
The long-term use of beta blockers remains a Class I
recommendation when given orally within 24 hours
to patients who do not have contraindications and are
not high risk for hypotension or cardiogenic shock.
In patients with left ventricular dysfunction, oral
beta blocker therapy is recommended but should be
gradually titrated.
Norepinephrine: Pregnancy Category C
Indication: Cardiac arrest and hypotension
Mechanism of Action: Norepinephrine is a sympath-
omimetic agent with both alpha and beta adrenergic
activity.
Dosing: The initial dose is 0.5 to 1 mcg/minute given
IV titrated to 8 to 30 mcg/minute. The dose is adjusted
according to the blood pressure.
Other things you should know about norepi-
nephrine:
Commonly Used Injectable Pharmacologic Agents 445
The solution should be given IV using a large vein.
Extravasation may cause sloughing and necrosis be-
cause of its
striction. After extravasation occurs, the area should
be immediately injected with 10 to 15 mL of saline
containing 10 mg of phentolamine.
Procainamide: Pregnancy Category C
Indication: Effective for both supraventricular and
ventricular arrhythmias. It is indicated for conversion
of atrial flutter and atrial fibrillation to normal sinus
rhythm, for control of ventricular rate in atrial fibrilla-
tion in the setting of WPW syndrome, and for stable
monomorphic wide complex tachycardia that may be
ventricular or supraventricular.
Mechanism of Action: Procainamide is a type IA
antiarrhythmic agent (Class I agents inhibit the fast
inward sodium channel causing a decrease in the maxi-
mum depolarization rate during phase 0 of the action
potential). It decreases automaticity by decreasing
the slope of spontaneous (phase 4) depolarization.
Procainamide also inhibits the potassium channel and
therefore prolongs the duration of the action potential.
Conduction velocity in the atrium, AV node, His-
Purkinje system, and ventricles is prolonged. The drug is
metabolized to N-acetylprocainamide (NAPA), which is
also an effective antiarrhythmic agent but has Class III
effects. Class III drugs prolong the action potential dura-
tion as well as refractoriness of cardiac tissues.
Dosing:
Procainamide is given IV at an infusion rate of 20 mg/
minute. The dose should not exceed 17 mg/kg. The
infusion is given until the arrhythmia is suppressed
or toxic complications from the drug is manifested
such as widening of the QRS complex by 50% when
compared with baseline, prolongation of the QT in-
terval or hypotension occurs.
When more rapid infusion is needed, an alternative
is to give intravenous boluses of 100 mg for 3 min-
utes every 5 minutes. The drug can also be given at a
faster infusion rate of 50 mg/minute, to a total dose
of 17 mg/kg during cardiac resuscitation.
Infusion is maintained at 1 to 4 mg/minute but
should be reduced if there is renal dysfunction.
Other things you should know about procainamide:
Is effective for both atrial and ventricular arrhythmias.
The drug should not be given to patients with pro-
longed QT interval.
Procainamide is negatively inotropic and is pro-
arrhythmic and should not be given to patients with
congestive heart failure or patients with systolic left
ventricular dysfunction (ejection fraction 40%).
LWBK271-App_435-448.qxd 29/1/09 9:34 pm Page 446 LWBK270-4119G-C02_073-110.qxd
446 Appendix
Hypotension can be precipitated if the drug is in-
jected too rapidly.
Unlike quinidine, another type IA antiarrhythmic
agent, procainamide does not increase digoxin levels.
The drug is metabolized to NAPA, which is also an
effective antiarrhythmic agent. When procainamide
blood levels are checked, NAPA levels should be in-
cluded. Therapeutic level of procainamide is 4 to 8
mcg/mL and for NAPA 7 to 15 mcg/mL.
The drug is mainly excreted through the kidneys un-
changed with a half-life of approximately 3 hours.
Excretion is delayed when there is renal dysfunction
or heart failure.
Blood levels should be checked when there is renal
dysfunction or maintenance infusion exceeds 2 mg/
minute or infusion exceeds 48 hours.
Can cause drug induced lupus when oral therapy is
continued for prolonged periods.
Propranolol (Inderal): Pregnancy
Category C
Indication: Propranolol has approved indications for
hypertension, angina pectoris, acute myocardial infarc-
tion, and treatment of cardiac dysrhythmias including
conversion of SVT to normal sinus rhythm.
Mechanism: Propranolol is a nonselective beta blocker
with 1- and 2-adrenergic blocking properties.
Dose: Approximately 1 to 3 mg is initially given. IV ad-
ministration should not exceed 1 mg/minute. Addi-
tional doses may be repeated after 2 minutes if needed.
The total IV dose should not exceed 10 mg adminis-
tered in three equal parts. The total dose can also be
given IV piggyback over 10 to 15 minutes. The IV dose
is followed by a maintenance oral dose of 180 to 320 mg
daily in divided doses.
Other things you should know about propranolol:
The elimination half-life of propranolol is 4 hours.
After the initial dose, additional IV doses should not
be given until after 4 hours after the last dose.
The drug is eliminated by hepatic metabolism.
Sotalol: Pregnancy Category B
Indication:
Sotalol is indicated in converting atrial fibrillation
to normal sinus rhythm in patients with WPW syn-
drome when the duration of the atrial fibrillation is
48 hours.
It is also indicated for monomorphic ventricular
tachycardia.
Mechanism of action: Sotalol is a Class III antiar-
rhythmic agent. Similar to amiodarone, it prolongs ac-
tion potential duration and increases refractoriness of
atrial and ventricular myocardium. It also has nonse-
lective beta blocking properties.
Dosing: The dose is 1 to 1.5 mg/kg given IV at 10
mg/minute.
Other things you should know about sotalol:
The intravenous preparation of sotalol is not avail-
able in the United States.
According to the American College of Cardiology/
American Heart Association/European Society of
Cardiology 2006 guidelines for the management of
patients with atrial fibrillation, sotalol is not effec-
tive for conversion of atrial fibrillation to sinus
rhythm but is effective for maintenance of sinus
rhythm and is used for preventing recurrence of
atrial fibrillation after the patient has converted to
normal sinus rhythm.
In patients with monomorphic VT, sotalol should
be given only when left ventricular systolic function
is preserved.
Sotalol has beta blocking properties. It should not be
given to patients who are already on beta blockers.
The intravenous infusion can cause bradycardia and
hypotension. Sotalol is also proarrhythmic and can
cause torsade de pointes.
Vasopressin (Pitressin): Pregnancy
Category C
Indication: VT/VF. Intended as an alternative to epi-
nephrine during cardiac resuscitation.
Mechanism of action: Vasopressin is a non-adrenergic
peripheral vasoconstrictor that is naturally present in
the body. It is an antidiuretic hormone. The agent be-
comes a powerful peripheral vasoconstrictor when given
in much higher doses than normally present in the body.
It does not have beta adrenergic activity and directly
stimulates non-adrenergic smooth muscle receptors. It
mimics the positive effects but not the adverse effects of
epinephrine and has a longer half-life of 10 to 20 minutes
compared with epinephrine, which is 3 to 5 minutes.
Dosing: A one-time bolus injection of 40 units given
IV during cardiac resuscitation for VT/VF. This substi-
tutes for epinephrine during resuscitation for cardiac
arrest, although epinephrine can still be given in re-
peated doses if necessary after 10 to 20 minutes if vaso-
pressin is not effective.
Other things you should know about vasopressin:
Vasopressin is a powerful non-adrenergic vasocon-
strictor given as a one-time dose of 40 units. It is
LWBK271-App_435-448.qxd 29/1/09 9:34 pm Page 447 LWBK270-4119G-C02_073-110.qxd
effective even in the presence of severe acidosis,
which commonly occurs during cardiac resuscita-
tion.
May be effective in asystole and pulseless electrical
activity.
Verapamil (Isoptin): Pregnancy
Category C
Indication: Conversion of paroxysmal supraventricu-
lar tachycardia to normal sinus rhythm, control of ven-
tricular rate in atrial flutter, or fibrillation or in patients
with multifocal atrial tachycardia.
Mechanism of action: Verapamil is a nondihydropy-
ridine calcium channel blocker that increases refrac-
toriness of the AV node. It can also slow down the rate
of the sinus node. It is a negative inotropic agent and
can decrease myocardial contractility resulting in
heart failure in patients with left ventricular dysfunc-
tion. It is also a peripheral vasodilator and can cause
hypotension.
Intravenous dose: The drug should not be given to
patient with left ventricular dysfunction. Give slowly
IV 2.5 to 5 mg over 2 minutes, longer in elderly pa-
tients, under continuous electrocardiogram and blood
pressure monitoring. If not effective, and no adverse
event is noted, repeat with another dose of 5 to 10 mg
every 15 to 30 minutes to a maximum dose of 20 mg.
Another option is to give 5-mg boluses every 15 min-
utes to a maximum dose of 30 mg.
Other things you should know about verapamil:
Nondihydropyridine calcium channel blockers such
as verapamil and diltiazem are very effective agents
in converting PSVT to normal sinus rhythm. They
are the next agents that should be used for conver-
sion of PSVT to normal sinus rhythm if adenosine is
not effective or is contraindicated.
Verapamil is a vasodilator and is negatively inotropic.
It should not be given to patients with left ventricular
dysfunction or patients with congestive heart failure.
Verapamil should be given only to paroxysmal
supraventricular tachycardia with narrow complexes
or supraventricular tachycardia with wide QRS com-
plexes with normal left ventricular function. When
there is wide complex tachycardia and the diagnosis
of the tachycardia is uncertain, verapamil should not
Commonly Used Injectable Pharmacologic Agents 447
be given. If the wide complex tachycardia turns out
to be ventricular, the administration of verapamil
may cause severe hypotension or even death.
Intravenous hydration and calcium chloride or cal-
cium gluconate IV may be given to counteract the
hypotensive effect of verapamil or diltiazem without
diminishing its antiarrhythmic effect.
Suggested Readings
2005 American Heart Association Guidelines for cardiopul-
monary resuscitation and emergency cardiovascular care.
Part 7.2: management of cardiac arrest. Circulation. 2005:
112;5866.
Antman EM, Hand M, Armstrong PW, et al. 2007 focused up-
date of the ACC/AHA 2004 guidelines for the management
of patients with ST-elevation myocardial infarction. J Am
Coll Cardiol. 2008;51:210247.
Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
ACC/AHA/ESC guidelines for the management of patients
with supraventricular arrhythmiasexecutive summary. A
report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines and the
European Society of Cardiology Committee for Practice
Guidelines. J Am Coll Cardiol. 2003;42:14931531.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006
guidelines for the management of patients with atrial fibril-
lationexecutive summary; a report of the American Col-
lege of Cardiology/American Heart Association Task Force
and the European Society of Cardiology Committee on Prac-
tice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (Writing Committee to
Revise the 2001 Guidelines for the Management of Patients
with Atrial Fibrillation). J Am Coll Cardiol. 2006;48:854906.
Hazinski MF, Cummins RO, Field JM, eds. AHA 2002 Handbook
of Emergency Cardiovascular Care. 4th ed. Dallas: American
Heart Association; 2002.
Micromedex Healthcare Series. Thomson Healthcare. http://
www.thomsonhc.com. Accessed January 2008.
Physicians Desk Reference. 62nd ed. Montvale: Thomson Health-
care Inc; 2008.
Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006
guidelines for management of patients with ventricular ar-
rhythmias and the prevention of sudden cardiac death: a re-
port of the American College of Cardiology/American Heart
Association Task Force and the European Society of Cardiol-
ogy Committee for Practice Guidelines (Writing Committee
to Develop Guidelines for management of patients with ven-
tricular arrhythmias and the prevention of sudden cardiac
death). J Am Coll Cardiol. 2006,48:e247e346.
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LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
Pages numbers in italics denote figures; those followed by a t denote tables.
Aberrant ventricular conduction, 168169, 170,
172173, 252, 310 (see also Rate related
bundle branch block)
Absolute refractory period, 3, 4, 8
Accelerated idioventricular rhythm (AIVR), 110,
125126, 154, 157, 162, 335, 352353,
367, 400, 402
Accelerated junctional rhythm, 109111, 154,
157, 162, 176177, 179, 220, 222, 224, 225
Accessory pathway (see Bypass tract)
Action potentials, 24, 7, 12, 13, 16, 1921, 72,
211, 224, 302, 337, 388, 407
of non-pacemaking cells, 211
of pacemaking cells, 211
Acute anterior MI, 86, 87, 98, 106, 109, 127, 128,
337, 349, 355, 356, 370, 371
Acute coronary syndrome, 331413
AV block, 352353
complications of acute MI, 350358, 351t
IV conduction defect, 354358
LBBB and, 357358
left anterior descending coronary artery
(LAD), 338341
left circumflex coronary artery (LCx), 341344
left ventricular dysfunction, 351t
non-ST elevation MI and unstable angina,
379413
other causes of ST elevation, 358364
primary angioplasty, 335337
RBBB and, 354356
right coronary artery (RCA), 344350
right ventricular MI, 249250, 251t
role of ECG in acute coronary syndrome,
331333, 379
ST-elevation MI, 331378
thrombolytic therapy, 334335
ventricular arrhythmias, 351352
ventricular arrhythmias, 351352
ventricular fibrillation, 351352
ventricular tachycardia, 351352
Acute inferior MI, 8688, 95, 98, 100, 106, 344,
346, 349, 350, 352, 353, 370373, 376
and AV block, 352
Acute myocardial infarction (see Acute
coronary syndrome)
Acute pulmonary embolism, 46, 64, 74, 76, 78,
127, 180
Adenosine, 165, 192, 196, 206209, 213,
215216, 225, 231, 235, 238, 243, 276,
280, 326, 328, 329t, 435
Advanced AV block (see Atrioventricular block)
Afterdepolarizations, 5, 185t, 224, 226
AIVR (see Accelerated idioventricular rhythm)
Aldosterone antagonist, 308t, 375, 394, 403
Algorithms
for diagnosing narrow complex tachycardia,
229
for wide complex tachycardia, 315
Alteplase, 373, 374, 394
Page 449 Aptara Inc
Index
Alternans (see Electrical alternans) common mistakes in, 249252
Amiodarone, 148, 197, 216, 220, 225, 226, 234, control of ventricular rate (see Rate control)
243, 244, 254259, 261t, 280, 281, 284, conversion to sinus rhythm (see Rhythm
302, 304307, 329t, 436437, 439 control)
Aneurysm (see Left ventricular aneurysm) ECG findings, 246248, 249
Angina (see Unstable angina) first detected, 248
Angiotensin-converting enzyme (ACE) incidence of, 165, 282
inhibitors, 254, 308t, 374, 375, 394, 403 lone, 248, 254, 261t
Angiotensin receptor blockers (ARB), 254, 308t, mechanism, 248
374, 375, 394, 403 nonvalvular, 248, 254
Anode, 420, 422, 432 pacemaker (see Pacemaker, cardiac)
Anterior MI, 28, 90, 118, 339, 341, 346, 350, 352, paroxysmal, 248
354, 366367, 370, 371 permanent, 248
and AV block, 355 persistent, 248
Anterograde conduction, 271, 272 prevalence, 246, 254
Antiarrhythmia devices, 111, 136, 147, 166, 377, prevention of stroke, 259260
433 rate control, 254256
Anticoagulation rhythm control, 257259, 437, 446447
in atrial fibrillation, 165, 259260 treatment of, 254260
in atrial flutter, 243 valvular, 248, 254
Antidromic atrioventricular reciprocating ventricular rate, 246247
tachycardia (AVRT), 198, 206, 273276, warfarin, 260, 261t
279, 280, 310, 314, 322, 327329 WPW syndrome and, 253, 256, 281285
Antitachyarrhythmia, 418t Atrial flutter, 233245
Antitachycardia devices, 244, 245, 430, 431 ablation of, 245
Antithrombotic agents, 259261, 375, 392 artifacts resembling, 242
ARP (see Atrial refractory period) atrial pacing, 244245
Arrhythmogenic right ventricular dysplasia atrial rate, 233, 243
(ARVD), (see Right ventricular dysplasia) common mistakes in, 236, 237241
Artery, coronary, 195, 333, 338, 340342, 344, complete AV block and, 235, 240
350351, 369, 371, 373, 376, 392 control of ventricular rate, 243244
dominant coronary, 341344, 346, 350, 371, 372 conversion to sinus rhythm, 244245, 442
posterior descending, 119, 339, 342, 344, electrical cardioversion, 245
346, 371 ECG findings, 233, 236
Ashman phenomenon, 252253 lone, 243, 245
Aspirin, 260261, 374, 378, 393t, 394 mechanism of, 233, 241
Asystole, 148, 151, 153, 154, 158 reverse typical, 233, 242
Atenolol, 196197, 225, 255, 437438 therapy, 243245
Atrial two to one block, 234, 237, 238, 239
contraction, 18, 19, 83, 106, 107, 195, 225, typical, 233, 241242
328, 352 ventricular rate, 234
deflection, 101 versus atrial tachycardia, 235, 238, 239
depolarization, 56 Atrial pacing (see Pacemakers, cardiac)
depolarization and repolarization, 57 rapid, 164, 244245
enlargement, 68 Atrial refractory period (ARP), 427428
escape rhythm, 153, 154, 167, 168 Atrial rhythm, 101, 236, 420, 421, 430
infarction, 351t, 372 chaotic, 154, 171, 219
ischemia, 372 Atrial septal defect, 78, 107, 225
left, 17, 66, 213, 214 repair, 208, 218
right, 65, 213, 214 Atrial tachycardia, 150, 152, 163, 169170, 174,
Atrial abnormality, left, 66, 68, 69, 71, 136 178, 186t, 209, 211, 212, 214216,
Atrial activation, 10, 100, 175, 204, 221, 262 226227, 231, 232, 235, 238, 239, 243, 436
left, 63, 64, 67 Atrial triggered pacemaker, 421
right, 63, 67 Atrioventricular block, 80111
Atrial fibrillation, 246261 acute MI and, 86, 93, 98, 99, 100, 352, 353,
Ashman phenomenon, 252 355, 356, 357, 375376
aspirin, 260, 261t, advanced second degree, 83, 9297, 93
atrial rate, 246 atrial fibrillation and, 252
classification, 248 atrial flutter and, 234235, 240
449
LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
450 Index
Atrioventricular block (continued )
classification of, 80
common mistakes in, 101, 102, 103
complete (see Third degree)
first degree, 8387, 104t, 145147
high grade (see Advanced second degree)
His recording and, 100101
indications for pacing, 104t, 104, 105, 107
infranodal, 8990
localizing site of, 85, 98, 100
nodal 8789
permanent pacing in, 104t
physical findings in, 105106
second degree, 8389
third degree, 97102, 104t, 104105
three to one, 93
treatment of, 9697, 107
two to one, 92, 93
type I (AV Wenckebach), 8389
type II (Mobitz II), 8992, 91, 8990, 92
Atrioventricular nodal reentrant tachycardia
(AVNRT), 185t, 187197, 199200, 202,
206, 207, 212, 215, 217218, 225,
227231, 238
Atrioventricular node, 9, 10, 112, 174, 263
Atrioventricular reciprocating tachycardia (see
Atrioventricular reentrant tachycardia
[AVRT])
Atrioventricular reentrant tachycardia (AVRT),
185t, 187, 190, 192, 194, 196, 198207,
212, 215218, 225, 227230, 272276,
278280, 282, 310
Atropine, 88, 89, 92, 96, 108109, 165, 180, 223,
371, 376, 438, 440, 441, 443
small doses of, 438
Atypical AVNRT, 190, 193, 194, 199, 215217,
227, 229231
Atypical AVRT, 199, 202, 203, 205, 206, 215217,
227231
Automatic cells, 7, 8, 181, 182, 186t, 292
Automatic defibrillator, 128, 308t, 309, 352, 355
Automaticity, 2, 7, 182, 439, 443, 445
enhanced, 181, 185186, 195, 211, 215216,
218, 220, 221, 224, 226, 301, 436
triggered, 209, 212, 226
AV block (see Atrioventricular block)
AV dissociation, 100, 106, 111, 251, 315,
317319, 328
AV junction, 7, 8, 19, 87, 9698, 104t, 105, 108,
109, 149, 153154, 161163, 167, 174176,
178, 179, 185t, 186t, 212, 224, 292
AV junctional escape rhythms, 97, 154
AV junctional rhythm, 88, 98, 107, 109, 153,
162, 220, 402
AV junctional tachycardia, 212, 215, 220
AV nodal ablation, 256
AV Wenckebach (see Atrioventricular block)
AVNRT (see Atrioventricular nodal reentrant
tachycardia)
AVRT (see Atrioventricular reentrant
tachycardia)
Bazett formula, 13, 20
Beta blockers, 148, 149, 182183, 196197, 207,
208, 215, 216, 220, 225, 243, 244,
254258, 304, 305, 307308, 374, 394,
436438, 440, 441, 445, 446
Page 450 Aptara Inc
Bi-atrial enlargement, 6566
Bidirectional ventricular tachycardia, 295, 298
Bifascicular block, 121, 122, 129, 134, 136, 138,
140142, 145146, 321, 323, 327
Bigeminy, 159160, 169, 170, 172173, 289, 290,
300
Bilateral bundle branch block, 138140, 145
Biphasic QRS complexes, 318, 316
Bipolar electrodes, 420, 422, 432
Biventricular hypertrophy, 46, 75, 77
Biventricular pacemakers, 136, 430433
Blocked premature atrial complexes, 101, 103,
158160, 164, 168170, 172174, 178
Bradycardia-dependent bundle branch block,
133134
Broad complex tachycardia (see Wide complex
tachycardia)
Brugada ECG, 304305, 309, 359, 361363
Brugada syndrome, 6, 21, 299, 301, 303304,
309, 362, 433
Bundle branch block, 120137
acute MI and (see Acute coronary
syndrome)
bilateral, 138, 139, 140, 141
incomplete LBBB, 72, 129
incomplete RBBB, 74, 124
left, 128137
rate related, 127, 131, 133, 134, 204206
right, 120128
Bundle branch reentrant tachycardia, 294
Burst pacing, 430, 431
Bypass tract, 263272
auscultatory findings, 271
concealed, 200, 206, 263264
location, 203205, 265269, 275276
manifest, 200, 206, 263
rapidly conducting, 199, 206
slowly conducting, 199, 206
Calcitonin, 409, 410
Calcium, 56, 20, 302, 396, 403, 404, 409, 410,
412, 438
Calcium channel blockers, 80, 106, 108, 146,
149, 183, 195197, 208, 215, 216, 243,
244, 254256, 258, 281, 285, 302, 394
nondihydropyridine, 183, 255
Calcium chloride, 404, 412, 447
Cardiac
markers, 332, 335, 346, 369
pacemakers, 414433
resynchronization therapy, 136, 137, 432
rotation, 3940, 46, 47
troponins, 333, 368, 369, 373, 379, 381, 383,
392
Cardiomyopathy, tachycardia-mediated, 212,
215, 216, 225, 226, 245, 256
Cardioversion, 257t, 260, 296, 305, 306, 431,
440, 442
direct current, 243245, 258, 259t, 284
Carotid sinus pressure, 158, 164, 195, 208, 235,
238, 250, 251, 280, 326, 327, 328
Cathode, 420, 422
Chamber enlargement and hypertrophy, 6279
bi-atrial, 6566
combined ventricular, 7577
left atrial, 6465, 6668
left ventricular, 6873
right atrial, 6264
right ventricular, 7375, 7778
Children, 13, 19, 20, 31, 40, 44, 117, 127,
212, 223, 225, 232, 246, 286, 299, 301,
379381
Chronic obstructive pulmonary disease
(COPD), 19, 46, 63, 73, 75, 116, 219, 220,
225, 254, 256
Chronotropic incompetence, 149, 163
Clockwise rotation, 4042, 46, 74, 77, 118, 367
Clopidogrel, 374, 378, 393t, 394, 445
Compensatory pause, 131, 169, 172, 173, 287,
296
Complete atrioventricular (AV) block, 80,
8690, 92, 96111, 127, 128, 136,
138139, 142, 143, 145148, 235, 236,
250, 252, 371, 423, 424, 427, 428, 431,
432 (see also Atrioventricular block)
Complete atrioventricular (AV) dissociation, 98,
99, 105107, 109111, 177, 178, 221, 224,
227228, 230, 250, 310, 311, 313, 314,
318, 321, 326, 327, 352, 357
Complete right bundle branch block (see
Bundle branch block)
Complete vagal blockade, 108, 376, 438
Concealed bypass tracts, 200, 204, 206, 207, 263,
285
Concealed conduction, 101, 103
Concordance
negative, 321, 322
positive, 321322
COPD (see Chronic obstructive pulmonary
disease)
Coronary arteries, 5, 61, 332, 333, 337339, 340,
341, 342, 343, 346, 350, 365, 370, 371,
385387, 392
Coronary vasospasm, 21, 332333, 368
Cough CPR, 165
Counterclockwise rotation, 4042
Coupling intervals, 174, 289, 293, 299301
long, 289
short, 289
Delta wave, 1516, 2122, 44, 200, 206,
263266, 269274, 276, 277, 279, 283,
284, 325, 367
negative, 265, 268, 279
Depolarization, 3, 68, 1012, 16, 20, 5561, 70,
72, 226, 302, 383, 385, 389, 390, 445
and repolarization, 5557, 59, 61, 126, 365
Diastole, 7, 1617, 21, 61, 69, 71, 107, 289, 389,
390
electrical, 1418, 388, 391
Diastolic depolarization, 134, 185t, 211, 226
slow spontaneous, 3, 7, 181
Digibind, 108, 439440
Digitalis, 5, 71, 80, 83, 87, 96, 106, 108, 179,
185t, 186t, 215216, 224227, 235, 239,
243244, 250, 251, 258, 280, 281, 285,
298, 301, 387, 403, 412, 439, 440
Digoxin, 195197, 207, 208, 244, 254258, 281,
285, 437440
dose of, 439
levels, 225, 258, 439, 440, 446
Diltiazem, 146, 174, 183, 196197, 208, 216, 220,
243, 244, 255257, 394, 437, 440, 447
Dipole, 5556
LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
Discordant ST segment depression, 358, 359
Disopyramide, 243, 257t, 280, 284, 302
Dobutamine, 89, 135, 165, 223, 225, 376,
440441, 443
Dofetilide, 257259, 302
Dual chamber pacemakers (see Pacemakers,
cardiac)
Early afterdepolarizations, 185t, 226
Early repolarization, 20, 359361, 382
Ebsteins anomaly, 127, 271, 329
Effective refractory period, 4, 8, 444
Electrical alternans, 5254, 203, 205, 216
Electrical axis, 29, 31, 32, 36, 47, 114, 117
and cardiac rotation, 30, 31, 33, 35, 37, 39, 41,
43, 47, 367, 379
Electrolytes, abnormalities, 21, 107, 174, 216,
299, 307, 308t, 329t, 352, 359, 361, 392,
396, 397, 399, 401405, 407, 409413
End-diastolic PVCs, 289
Endocardium, 2, 6, 11, 2021, 57, 5961, 68, 69,
7172, 112, 126, 327, 385, 390391
Enoxaparin, 374, 393
Epicardial cells, 6, 20, 21, 61, 304, 391
potential duration of, 21, 390
Epicardium, 4, 6, 11, 20, 21, 5761, 68, 69, 71,
72, 126, 327, 362, 383, 385, 390391
Epinephrine, 89, 92, 96, 108, 165, 180, 303, 305,
438, 441, 444, 446
Epsilon wave, 16, 21, 22, 28
Equiphasic, 3134, 36, 37, 3942
Erythromycin, 302
Escape
beats, 94, 96
interval, 417t, 419420
rhythm, 87, 88, 92, 97100, 102, 104106,
108, 146, 149, 153, 154, 161163
Esmolol, 196, 197, 225, 244, 255, 257t, 438, 441,
442
Exit block, 149151, 163
Fascicular Block, 47, 92, 112113, 117, 119121,
127, 145147, 321, 327, 351t, 355,
366, 371
alternating, 138, 145
Fast sodium channels, 58, 302, 303
First-degree AV block, 8083, 89, 99, 107, 139,
143, 145147
First diagonal branch, 339343, 351t, 366, 370
Flecainide, 216, 225, 243, 244, 257259, 276,
279, 280, 284, 304, 329
Flutter, atrial (see Atrial flutter)
Flutter, ventricular, 294, 297, 299
Focal atrial tachycardia, 190, 194, 196, 209,
211218, 225, 227232, 279, 280, 436
Focal atrial tachycardia junctional tachycardia,
228
Focal junctional tachycardia, 221, 223226, 231
Fondaparinux, 374, 393
Frontal plane, 24, 2627, 3032, 36, 5860,
6265, 116, 121123, 145, 180, 269, 270,
289, 291, 292, 298, 346, 379380
Fully compensatory pause, 288, 289
Fusion complexes, 262, 271, 276, 282, 289, 293,
294, 299, 311314, 327, 397, 404406,
408
wide complex tachycardia, 312
Page 451 Aptara Inc
Ground electrode, 2428
Group beating, 8586
Heart block (see Atrioventricular block)
rate, 1214, 2021, 4851, 53, 89, 96, 107, 108,
134, 149, 182, 247249, 252, 255, 256,
298, 299, 360361, 437441
rate and voltage, 48, 49, 53, 234
rate meter stick, 49, 51
rate table, 49
rates, calculating, 49
Heparin, 374, 375
His-Purkinje
cells, 2, 7
system, 3, 5, 7, 10, 14t, 15, 18, 21, 81, 85, 90,
91, 94, 96, 105, 146, 168, 444, 445
Hisioventricular fiber, 285
Horizontal plane, 27, 30, 36, 38, 39, 5860, 62,
63, 65, 180, 342, 379, 380
Hypercalcemia, 16, 20, 216, 396, 408410, 413
Hyperkalemia, 21, 148, 158, 163, 179, 305, 359,
361, 381382, 396397, 401404,
407408, 411, 412
severe, 397, 399404
treatment of, 403
Hypersensitive carotid sinus syndrome, 158,
163, 164, 441
Hypertension, 21, 67, 70, 7273, 79, 117, 119,
127, 134136, 146, 243, 248, 254, 255,
260, 261t, 374, 441446
Hypocalcemia, 299, 396, 397, 402, 409413
symptoms of, 412
Hypokalemia, 14t, 15, 21, 216, 225, 299, 302,
304, 307, 396, 404408, 410, 412, 413
Hypomagnesemia, 216, 220, 299, 302, 307, 407,
412, 444
Hypothermia, 16, 20, 22, 107, 148, 305, 359, 362,
364, 438
Hysteresis, 417t, 419, 420
IART (see Intra-atrial reentrant tachycardia)
Ibutilide, 197, 244, 256259, 276, 279281, 284,
302, 329t, 442443
ICD (see Implantable cardioverter defibrillator)
Idiopathic Hypertrophic Subaortic Stenosis
(IHSS), 367
IHSS (see Idiopathic Hypertrophic Subaortic
Stenosis)
Implantable cardioverter defibrillator (ICD),
375376, 431433
Inappropriate sinus bradycardia, 149, 159, 161,
163
Inappropriate sinus tachycardia, 180183, 212
Incomplete LBBB, 128, 129, 298
Incomplete RBBB, 124, 127
Increased voltage, 19, 6869, 71, 72, 76, 77
Inferior myocardial infarction (MI), 44, 45, 113,
115117, 119, 344, 346, 350, 354, 366,
370, 372
and AV Block, 352
diagnosis of, 366
Infranodal block, 86, 8889, 9294, 96, 98100,
102, 106, 109, 138, 375, 438, 440, 441, 443
Injury
diastolic current of, 386, 388391
subendocardial, 342, 344, 345, 385, 386, 389,
391
INR (see International normalized ratio)
Index 451
Insulin, 403, 404, 407
Intermittent preexcitation, 264, 272
Intermittent right bundle branch block, 125, 126
International normalized ratio (INR), 260261,
373
Internodal tracts, 4
Intra-atrial block, 6668
Intra-atrial reentrant tachycardia (IART), 187,
207209, 218
Intra-atrial reentry, 186t, 215
Intracellular potassium, acute shift of, 402, 403
Intraventricular conduction defect, 20, 42, 47, 112,
113, 117, 119121, 125, 127, 129, 131, 133,
135139, 355, 370372, 375, 376, 432
Intraventricular conduction system, 12, 9, 10,
57, 87, 92, 105, 112, 125, 134, 272, 370
Intrinsicoid deflection, 57, 58
Ionized calcium, 408, 409, 412
level of, 409, 412
normal level of, 410, 412
Ischemia, myocardial (see Myocardial ischemia)
Isoproterenol, 89, 92, 96, 165, 174, 304, 307, 441,
443
J point, 11, 12, 15, 18, 20
J point elevation, 20
J wave, 20 (see also Osborn wave)
JT interval, 18, 412
Jugular venous pulse, 105108
Junctional escape rhythm, 88, 9799, 106,
154155, 158, 161
Junctional rhythm, 98, 100, 110, 155, 176178,
224, 225, 397
accelerated, 176177, 722
Junctional tachycardia, 105, 109111, 176, 177,
186t, 193, 209, 212, 215, 217, 220221,
223, 224, 227232
automatic, 221, 225
Juvenile pattern (see Persistent juvenile pattern)
Ketonazole, 302
L-type calcium channels, 302, 304
LAD (see Left anterior descending)
LAFB (see Left anterior fascicular block)
Late afterdepolarizations, 185t, 226
Late impulses, 167, 168
Late transition, 4042, 46
Lateral MI, 117, 118, 342, 367
LBBB (see Left bundle branch block)
LCx (see Left circumflex)
Left anterior descending (LAD), 31, 291,
338343, 350351, 370371
coronary artery, 119, 127, 336338, 343, 366,
377
Left anterior fascicle, 2, 10, 112114, 116, 117,
119, 127, 292, 298
Left anterior fascicular block (LAFB), 28, 47, 72,
86, 99, 113117, 119123, 125, 127, 132t,
133, 138142, 144145, 354, 356
diagnosis of, 114
Left atrial
conduction delay, 136
enlargement, 6468, 79
origin, 213, 214
pressure, 17, 71
tachycardia, 215
LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
452 Index
Left axis deviation, 30, 31, 68, 69, 7172, 113,
115117, 119, 122, 123, 130, 133, 145,
269, 270, 291, 293, 320, 321, 327, 356
Left bundle branch block (LBBB), 90, 91, 112,
127141, 145, 146, 205, 206, 266, 267,
289, 291292, 318321, 323, 334335,
357359, 361362, 366368, 371372,
432, 433
configuration, 276, 278, 322, 422 (see also
pattern)
pattern, 269, 401
Left circumflex (LCx), 4, 5, 338346, 350351,
370372, 377, 386
coronary artery, 4, 5, 345, 370, 386
Left posterior fascicle, 2, 10, 112114, 116, 117,
119, 121, 129, 134, 138, 293, 295, 298
Left posterior fascicular block (LPFB), 113,
116118, 120, 122123, 132t, 138, 141,
144, 353, 354
diagnosis of, 117, 119
Left-sided bypass tract, 204, 265268, 271, 276,
279, 285
Left-sided posteroseptal bypass tract, 268, 269,
279, 283
Left ventricular aneurysm, 359, 363, 365
hypertrophy (LVH), 6, 19, 21, 46, 58, 6773,
7679, 116, 117, 129, 133, 135, 266, 267,
359, 361362, 366, 385387
hypertrophy, regression of, 72, 73
origin of PVCs, 292
strain, 6871, 385
Lidocaine, 306307, 329t, 444
Limb electrodes, 24, 26, 27, 52
Long QT syndrome, 22, 299, 301304, 307, 309,
433
Low voltage, 19, 46, 52, 77
LPFB (see Left posterior fascicular block)
LVH (see Left ventricular hypertrophy)
Magnesium deficiency, 444
Mahaim fibers, 285
Management of ST elevation MI, 375, 376, 445
Manifest bypass tracts, 200, 206, 207
MAT (see Multifocal atrial tachycardia)
Metoprolol, 196197, 225, 244, 255, 257t,
437438, 444445
MI (see Myocardial infarction)
Mitral
regurgitation, 70, 129, 135, 136, 254, 372,
392
stenosis, 46, 67, 73, 78, 254, 260
valve, 17, 6769, 71, 106, 259t, 339
Monomorphic VT, 294, 299, 305308, 329t, 446
Monophasic shock, 306308
Morphine sulfate, 374, 394
Multifocal atrial rhythm, 169, 171, 219
Multifocal atrial tachycardia (MAT), 169, 171,
212, 218220, 227229, 232, 250, 251,
436, 440, 447
Muscle cells, 13, 58, 10, 12, 15, 19, 55, 56, 61,
98, 125, 126, 167, 263, 274, 327
Myocardial infarction (MI), 8587, 99, 100, 115,
116, 127, 128, 135, 146, 323, 324, 327, 328,
342345, 347348, 350, 351t, 353359,
366368, 371373, 376379, 395
acute anteroseptal, 99, 339, 353, 356, 358
Myocardial injury, 383, 385, 386, 388, 390392
Page 452 Aptara Inc
Myocardial ischemia, 379395
non-ST elevation MI, 379395
ST depression, 383387
ST elevation, see ST-elevation MI, 383
ST segment in, 383390
subendocardial, 380381, 382,, 383, 385
T waves in, 380381
transmural, 380381, 383, 384
unstable angina, 379395
Myocardial necrosis, 332, 334, 368, 369, 373,
379, 390392
Myopotentials, 417t, 419
Narrow complex AVRT, 198, 199, 204206,
272273, 276, 278
Narrow complex tachycardia (see
supraventricular tachycardia)
Nitroglycerin, 332, 333, 368, 373, 374, 376, 394
Non-ST elevation myocardial infarction (MI),
331, 332, 337, 365, 369, 374, 376, 379,
381, 383, 386, 391394
and unstable angina, 21, 379, 381, 383, 385,
387, 389, 391, 393t, 395
Nondihydropyridine calcium channel blockers,
148, 174, 197, 208, 220, 225, 244,
255257, 440, 447
Nonparoxysmal junctional tachycardia, 179,
186t, 212, 220226, 228
Nonsustained VT, 294, 301, 308t, 309, 376, 433
(see also Ventricular tachycardia)
Norepinephrine, 180, 445
Normal AV conduction system, 80, 167, 173,
175, 184, 188, 198, 209, 215, 220, 262,
269, 271, 273, 310
Normal axis, 3031, 39, 116, 136, 291
Normal quadrant, 30, 31
Normal rotation, 40, 41
Normal sinus rhythm, 189192, 196, 200202,
206208, 213, 235, 242245, 254260,
265266, 270273, 298299, 322325,
327, 435438, 440443, 445447
Orthodromic AVRT, 198, 205207, 273, 274,
276, 281
Osborn wave, 1516, 2022, 362, 364, 408
Overdrive pacing, 186t, 307, 431
Oversensing, 417t, 419, 432
P-mitrale, 6467, 69
P-pulmonale, 62, 64, 7375, 77
Pacemakers, cardiac, 414433
atrial demand, 416, 420, 421
atrial fibrillation, 256, 419, 424, 426
atrial flutter, 244, 245, 426, 429
atrial fixed rate, 416, 420
atrial, single chamber 414415
atrial synchronous, 428
biventricular, 432
cardioverter/defibrillators, 418t, 430431,
433
demand, 415, 417
dual chamber, 423426
electrodes, 420422
bipolar, 420, 422
unipolar, 422
fixed rate, 415, 417
hysteresis, 417, 419, 420
indications for, 104t, 146147, 159, 162
AV block, 104t
IV conduction defect, 146147
sinus node dysfunction, 159, 162
modes, 416421, 424426, 428430
AAI, 416, 417t 420, 421
AAT, 416, 417t, 420, 421
A00, 416, 417t, 420, 421
DDD, 424426, 429
DDI, 430
DVI, 428, 429
VAT, 428, 429
VDD, 428, 429, 430
V00, 416, 417, 418, 419
VVI, 416, 417, 418, 419
VVIR, 416
VVT, 416, 419, 420, 421
mode switching, 429
oversensing, 417
Pacemaker-induced left bundle branch block
pattern, 422
Pacemaker-induced right bundle branch block
pattern, 422, 423
Pacemaker mediated tachycardia (PMT),
427428, 432
sinus tachycardia and DDD pacing, 426,
428
syndrome, 83, 88, 104t, 225, 422, 423, 431, 432
temporary, 92, 169, 307, 440, 443
triggered (see AAT and VVT)
ventricular demand, 415416,
ventricular fixed rate, 415, 418
ventricular, single chamber, 414,
ventricular tachycardia, 430, 431, 433
Pacemaker-induced QRS complexes, 45
PACs (see Premature atrial complexes)
Pamidronate, 410
Papillary muscle rupture, 351t, 372
Papillary muscles, 135, 136, 339, 342, 343, 350,
351
Parasystolic impulses, 294, 301 (see also
Ventricular parasystole)
Paroxysmal atrial tachycardia (see Paroxysmal
supraventricular tachycardia)
Paroxysmal junctional tachycardia, 212, 223, 225
(see also Paroxysmal supraventricular
tachycardia)
Paroxysmal supraventricular tachycardia, 210,
435, 440, 447
Pathologic Sinus Tachycardia, 180, 181, 183, 211
PCI (see Percutaneous coronary intervention)
Peak time (see R peak time)
Percutaneous coronary intervention (PCI), 127,
334, 336, 373375, 379, 392, 393
Pericardial effusion, 5354, 69
Pericarditis, 164, 182, 254, 359361, 381, 391
acute, 21, 359, 362364, 377
Permanent atrial fibrillation, 248
Permanent pacemakers (see pacemakers, cardiac)
Persistent atrial fibrillation, 257t, 258, 261
Persistent juvenile pattern, 380, 381
Phenytoin, 225, 307
PJC (see Premature junctional complex)
PMT (see Pacemaker-mediated tachycardia)
Polymorphic ventricular tachycardia (PVT),
295299, 307309, 442 (see also
Ventricular tachycardia)
LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
Posterior MI, 44, 342344, 367
Posterolateral MI, 342, 345, 347, 348, 371, 372, 386
Posterolateral wall, 338, 341, 342, 345, 347, 350,
370, 371
Posteroseptal area, 203, 206, 266, 267
Postural orthostatic tachycardia syndrome
(POTS), 181183
Potassium
channel, 6, 303, 436, 442, 444, 445
transport, 303304
Potassium level serum, 361, 397, 403404, 407
Potential duration, 6, 59, 61, 134, 301, 304, 383,
390, 442, 444446
POTS (see Postural orthostatic tachycardia
syndrome)
PR interval, 12, 15, 18, 19, 8087, 8996
normal, 81, 82
PR segment, 15, 19
Precordial electrodes, 27, 36, 3947, 53, 59, 339
right-sided, 348
Precordial thump during ventricular fibrillation,
305
Preexcitation, 16, 200, 206207, 253, 255, 262265,
270272, 276283, 285, 311, 313, 322,
324, 325, 327, 328, 367, 381 (see also
Wolf-Parkinson-White syndrome)
Premature atrial complexes (PACs), 101, 103,
158160, 164, 167174, 176, 178179,
181, 188, 198, 207, 241, 248, 250, 253,
273274
aberrantly conducted, 168170, 172
nonconducted, 159, 160, 164, 168, 172
Premature junctional complex (PJC), 167,
174179
Premature supraventricular complexes (see
Premature atrial complexes)
Premature ventricular complexes, 101, 287,
289293
Pressure overload, 64, 7072, 78
Procainamide, 197, 216, 243, 244, 256, 257t, 276,
279281, 283, 284, 302, 304, 306, 307,
329t, 445446
Propafenone, 197, 216, 225, 243, 244, 257259,
280, 281
Propranolol, 183, 196197, 225, 244, 255, 437,
438, 446
Pulmonary disease, 62, 64, 117, 119, 174, 243,
245, 248, 260
Pulmonary hypertension, 46, 64, 68, 78, 107,
120, 127
Pulmonary veins, 1, 172, 211, 212, 215, 225, 232,
241, 242, 249, 253, 256, 259
Purkinje fibers, 1, 2, 1011, 57, 61, 112, 114, 383,
385, 390, 404
network of, 2, 5, 57, 112, 116, 119
PVCs (premature ventricular complexes), 131,
168, 169, 171174, 287294, 298301,
308t, 309
PVT (see Polymorphic ventricular tachycardia)
QRS axis, 3639, 72, 73, 77, 113, 114, 116, 117,
119, 122, 127, 321, 380
normal, 30, 31
QT dispersion, 20, 301
QT interval, 1218, 20, 258, 296, 299, 301303,
307, 381, 391, 396, 397, 401, 404408,
410, 412, 442, 444, 445
Page 453 Aptara Inc
corrected, 13, 402
long (see QT prolongation)
normal, 298, 404, 407
prolonged, 20, 298, 302, 412, 444, 445
short, 303, 397, 408
QT prolongation, 299, 302, 307, 436
QTc (see QT interval)
QTc interval (see QT interval)
Quadrants, 30, 31
northwest, 30, 74, 75, 77
Quadrigeminy, 289, 290
Quinidine, 21, 234, 243, 257259, 280, 284, 302,
304, 439, 446
R peak time, 58, 88, 120, 125126, 128, 132
R-P Interval, 201, 230
R-R Interval, 13, 14
Radiofrequency ablation (RA), 127, 183, 206,
208, 231, 242, 245, 256, 278, 281,
284286, 298
Rate-related bundle branch block, 131, 133, 135,
204205, 205, 310
RBBB (see Right bundle branch block)
RCA (see Right coronary artery)
Reciprocal ST depression, 304, 337339, 341,
342, 344348, 360, 362, 370372
Reentrant junctional tachyarrhythmias, 210,
232
Refractory period, 34, 8
absolute, 34, 8
effective, 4, 8
relative, 4, 8
Relative refractory period, 4, 8
Repolarization, 38, 12, 1416, 18, 2021, Single chamber ventricular pacemakers, 414,
5557, 5961, 70, 72, 224, 289, 301, 302,
304, 383, 385, 390
direction of, 60, 383, 385
wave, 19, 5557, 60, 383, 385, 391
Resting potential, 38, 12, 55, 211, 302, 386,
388389, 402, 406
Retrograde conduction, 107, 224, 272, 274, 289,
329t, 422, 423, 427 (see also
ventriculoatrial conduction)
Reverse typical, atrial flutter, 233, 242
Right atrial enlargement, 6266, 7477, 118
Right atrial pressure, 107
Right axis deviation, 30, 31, 44, 46, 73, 74,
7678, 116117, 119, 122, 123, 130, 145,
291, 292, 321, 327
Right bundle branch block (RBBB), 4243, 98,
99, 112, 119128, 132t, 134136,
138141, 144145, 205, 291293, 295,
310, 316, 319, 351352, 354356,
371372
configuration, 157, 169, 275, 278, 322, 422,
423
pattern, 252, 318, 363
preexistent, 322, 324
Right coronary artery (RCA), 4, 5, 338339, 342,
344, 346351, 370372
Right-sided anteroseptal bypass tract, 269, 270
Right-sided bypass tract, 204, 205, 265269, 271,
276, 277
Right-sided posteroseptal bypass tract,
268269
Right-sided precordial leads, 38, 58, 77, 125,
132t, 134, 304, 348350, 372, 373
Index 453
Right ventricular cardiomyopathy (see Right
ventricular dysplasia)
Right ventricular
dysplasia, 16, 22, 28
hypertrophy (RVH), 4244, 46, 58, 69, 7375,
7778, 107, 116120, 127, 271
infarction, 107, 371, 372
MI (RVMI), 28, 331, 346, 349351, 372373,
376
PVCs, 289, 291292
Roller coaster ECG configuration, 406
Rotation, 30, 39, 40, 78
RVH (see Right ventricular hypertrophy)
RVMI (see Right ventricular MI)
Saddleback ECG pattern (see Brugada ECG)
SART (see Sinoatrial Reentrant Tachycardia)
Second-degree AV block (see Atrioventricular
block)
Secondary ST segment depression, 386
Septal activation 5859, 60, 126, 134
Septum, 5860, 107, 126, 134, 338
Serum calcium, 408412
normal level of total, 408, 409
Serum potassium, 305, 382, 396, 397, 401,
403404, 407
Shortened PR interval, 270
Sick sinus syndrome, 102, 148150, 153, 158,
161, 163166, 244, 258, 415, 432, 435,
440, 442, 443
Signal, calibration, 48, 52
Sine waves (see Waves, sine)
Single chamber atrial pacemaker, 414416, 432
415, 431, 432
Sinoatrial exit block, 149151, 161
Sinoatrial reentrant tachycardia (SART), 182,
187, 207208, 227230
Sinoventricular rhythm, 397, 399, 402
Sinus
arrest, 101102, 149151, 159161, 163, 168,
169, 172, 443
arrhythmia, 9, 93, 150, 159161, 164
arrhythmia, ventriculophasic, 93, 94
bradycardia, 9, 149, 159, 160, 163, 164, 172,
173, 351t, 364, 370, 372
inappropriate, 149, 159, 161, 163
node cells, 24, 182, 183, 211
node dysfunction, 148166
pauses, 149, 150, 155, 159161, 163165, 172,
174
Sinus tachycardia, 9, 21, 74, 76, 131, 180185,
195, 206208, 213215, 226230, 335,
370, 424428, 430431, 445
inappropriate, 180183, 212
physiologic, 181, 211
and SART, 230
Slow pathway (SP), 185t, 188190, 192194,
196, 198, 199, 206
Sodium bicarbonate, 403, 404
Sodium channel blockers, 304, 377, 436
Sodium channels, 7, 303, 362, 444
Sodium ions, 3, 57, 302, 303
Sotalol, 148, 216, 225, 234, 239, 244, 257t, 258,
261t, 280, 281, 302, 306, 307, 329t, 438,
446
SP (see Slow pathway)
LWBK271-Ind_449-454.qxd 03-02-2009 08:32 PM
454 Index
Spontaneous depolarization, 4, 7
ST-elevation myocardial infarction, 331378,
388389 (see also Acute coronary
syndrome)
ST segment depression, 70, 71, 73, 127, 239, 341,
347, 357, 368, 369, 373, 379, 385387,
389392
concordant, 124, 130, 354, 355, 356, 357
discordant, 124, 130, 354, 357358
in V1 to V3, 342, 344, 345, 371, 372
ST segment elevation, 2021 (see also Acute
coronary syndrome)
concordant, 135, 356, 358
discordant, 135, 358, 359
in normal individuals, 2021
Statins, 375, 394, 437
Stents, bare metal, 374, 393
Strain, acute right heart, 74, 76
Streptokinase, 373, 374, 394
Subendocardial ischemia, 380383, 385,
391
Sudden death, 79, 97, 106, 146, 153, 162164,
281283, 298, 299, 301305, 308309, Unipolar leads, 2427
352, 371, 377, 378
Superconducting AV node, 286
Supernormal phase, 4, 8
Supraventricular tachycardia (SVT), 184232
algorithm, 228231
enhanced automaticity, 211226
mechanism, 184186
reentry, 187210
triggered activity, 226227
SVT (see Supraventricular tachycardia)
Syncope, 97, 106, 146, 150, 153, 162164, 166,
195, 208, 293295, 299, 303305, 328,
362, 419, 422
T-waves, 21, 379383
abnormal, 380383
normal, 21, 379380
T-wave infarct, 381, 383, 391
T-wave inversion, 331, 368, 369, 379, 380,
383385, 392
Tachycardia (see individual tachycardias)
Tachycardia-bradycardia syndrome, 148150,
152, 153, 161, 163
Takotsubo cardiomyopathy, 359, 363
Tall QRS complexes in V1, 77
Tall voltages, 52, 53, 70, 76, 133, 135
TARP (see Total atrial refractory period)
Tenecteplase, 374, 394
Theophylline, 165, 174, 186t, 196, 207, 215, 216,
219, 435
Thrombolytic therapy, 331, 334336, 342, 365,
371, 373375, 377, 385, 386
Tombstoning electrocardiographic pattern,
377
Torsades de pointes, 20, 244, 258, 294299, 302,
307, 406, 407, 442444, 446
Total atrial refractory period (TARP), 428
Total QRS voltage, 70, 71
Page 454 Aptara Inc
T-P segment, 21
TQ segment, 1517, 21, 388390
Transcutaneous pacing, 108, 438
Transition, early, 4042
Transition zone, 3941, 46, 73, 78, 359360
Transmural myocardial necrosis, 365, 366,
391
Transvenous pacing, 108, 438
Tricuspid regurgitation, 78, 107
Trifascicular block, 119, 136141, 143147,
356
Trigeminy, 169, 170, 289290, 300
Triggered activity, 185t, 184186, 226227
Triphasic, 169, 322, 324
Troponins, 335, 369, 373, 381, 392
Typical atrial flutter, 233, 234, 241, 242, 245
Typical AVNRT, 190, 194, 199
Typical AVRT, 199, 201, 202, 205, 206
U wave, 13, 14, 15, 18, 21 (see also
hypokalemia)
Unfractionated heparin, 374, 393
Unipolar electrodes (see Pacemakers, cardiac)
Unstable angina, 331, 332, 337, 369, 374, 377,
379395
Upright flutter waves, 238, 241
Vagal maneuvers for terminating SVT, 195196
Vasopressin, 305, 438, 446
VAT (see Ventricular activation time)
Ventricular
aberration, 184, 252, 253, 310, 321, 323
escape rhythm, 88, 92, 98100, 106, 109,
138139, 142143, 145, 146, 154156,
236, 252
fibrillation (VF), 297301, 304, 305, 308t, 309,
351t, 352, 370372, 376, 412, 433, 435,
436, 444, 445
flutter, 294, 298300, 397
fusion, 155, 310314, 326
gradient, 395
muscle cells, 24, 7, 12
parasystole, 292294, 299301, 308
Ventricular activation time (VAT), 58, 69, 71, 72,
78, 126
Ventricular arrhythmias (see also Ventricular
tachycardia, Ventricular flutter,
Ventricular fibrillation)
classification, 293294
end diastolic, 289
interpolated PVC, 288
parasystole, 292
paired, 289
premature ventricular complexes (PVC),
287292
trigeminy, 289
Ventricular pacing (see Pacemakers, cardiac)
Ventricular repolarization, 12, 21, 57, 59, 60, 72,
301, 404
rapid, 6, 12
Ventricular rhythms, 106, 109, 111, 162164,
352, 414
accelerated, 109, 111, 397
Ventricular tachycardia (VT) (see also Wide
complex tachycardia), 293309
bidirectional, 295, 298
Brugada syndrome, 303304
bundle branch reentry, 294, 298
cardioverson, electrical,306
classification, 293, 294
diagnosis of, 310330
long QT, 301303
monomorphic VT, 294, 300, 305
nonsustained, 294, 308
polymorphic VT, 294300, 306307
sustained, 294, 301, 305306, 307308
temporary pacing, 306
torsades de pointes, 295, 296, 299300, 306
Ventriculoatrial conduction, 157, 274, 280, 287,
289, 310, 314, 326, 423, 427, 432
Verapamil, 146, 183, 196197, 206, 208, 215,
216, 220, 232, 235, 243, 244, 255256,
278, 285, 302, 440, 447
VF (see Ventricular fibrillation)
Voltage discordance, 76, 77
VT (see Ventricular tachycardia)
Wandering atrial pacemaker, 154, 156, 159, 161
Warfarin, 254, 256, 258261, 437
Waves, sine, 397, 399, 402
Wide complex
AVRT, 272276, 278, 280, 314, 327
SVT, 310, 314, 319, 321, 322, 326328, 436
Wide complex tachycardia, 310330 (see also
ventricular tachycardia)
causes of, 310
diagnosis with rhythm strip, 310314
diagnosis with 12 lead ECG, 314330
favors VT, 310321, 326
favors SVT, 321322, 327
of uncertain diagnosis, 278
of unknown origin, 435, 436, 440
physical findings, 324, 328
treatment, 328329, 435, 436, 445
wide complex AVRT (see WPW syndrome)
Wolf-Parkinson-White (WPW) Syndrome,
262286
and atrial fibrillation, 253, 256, 281285
antidromic AVRT, 273281
Auscultatory findings in, 271
localizing the bypass tract
during sinus rhythm, 265272
during narrow complex AVRT, 203205
during wide complex AVRT, 275276
narrow complex AVRT, 198207
orthodromic AVRT, 198207
wide complex AVRT, 273281
Women, 13, 20, 27, 68, 71, 134, 187, 243, 299,
302, 305, 374, 375, 439
WPW syndrome (see Wolff-Parkinson-White
[WPW] syndrome)